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        <title>Circulation Research via MedWorm.com</title>
        <description>MedWorm.com provides a medical RSS filtering service. Over 6000 RSS medical sources are combined and output via different filters. This feed contains the latest items from the 'Circulation Research' source.</description>
        <link><![CDATA[http://www.medworm.com/rss/search.php?qu=Circulation+Research&t=Circulation+Research&s=Search&f=source]]></link>
        <lastBuildDate>Wed, 08 Feb 2012 09:32:34 +0100</lastBuildDate>
        <item>
            <title>Necl-5/Poliovirus Receptor Interacts With VEGFR2 and Regulates VEGF-Induced Angiogenesis.</title>
            <link>http://www.medworm.com/index.php?rid=5642916&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22282193%26dopt%3DAbstract</link>
            <description>Conclusions:These results demonstrate the critical role of Necl-5 in angiogenesis and suggest that Necl-5 may regulate the VEGF-induced angiogenesis by controlling the interaction of VEGFR2 with integrin α(v)β(3), and the VEGFR2-mediated Rap1-Akt signaling pathway.
    PMID: 22282193 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5642916</comments>
            <pubDate>Thu, 26 Jan 2012 05:00:00 +0100</pubDate>
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        <item>
            <title>Selective Class I Histone Deacetylase Inhibition Suppresses Hypoxia-Induced Cardiopulmonary Remodeling Through an Antiproliferative Mechanism.</title>
            <link>http://www.medworm.com/index.php?rid=5642915&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22282194%26dopt%3DAbstract</link>
            <description>Conclusions:By targeting distinct pathogenic mechanisms, isoform-selective HDAC inhibitors have potential as novel therapeutics for pulmonary hypertension that will complement vasodilator standards of care.
    PMID: 22282194 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5642915</comments>
            <pubDate>Thu, 26 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5642915</guid>        </item>
        <item>
            <title>Extrinsic Notch Ligand Delta-Like 1 Regulates Tip Cell Selection and Vascular Branching Morphogenesis.</title>
            <link>http://www.medworm.com/index.php?rid=5642914&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22282195%26dopt%3DAbstract</link>
            <description>Conclusions:Dll1 acts as an extrinsic cue involved in tip cell selection, which directs vessel sprouting and branch formation.
    PMID: 22282195 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5642914</comments>
            <pubDate>Thu, 26 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5642914</guid>        </item>
        <item>
            <title>High Levels of Co-Stimulatory Receptors OX40 and 4-1BB Characterize CD4+CD28null T Cells in Patients With Acute Coronary Syndrome.</title>
            <link>http://www.medworm.com/index.php?rid=5642913&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22282196%26dopt%3DAbstract</link>
            <description>Conclusions:Costimulatory pathways are altered in CD4(+)CD28(null) T cells in ACS. We show that the inflammatory and cytotoxic function of CD4(+)CD28(null) T cells can be inhibited by blocking OX40 and 4 to 1BB costimulatory receptors. Modulation of costimulatory receptors may allow specific targeting of this cell subset and may improve the survival of ACS patients.
    PMID: 22282196 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5642913</comments>
            <pubDate>Thu, 26 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5642913</guid>        </item>
        <item>
            <title>Hyperamylinemia Contributes to Cardiac Dysfunction in Obesity and Diabetes: A Study in Humans and Rats.</title>
            <link>http://www.medworm.com/index.php?rid=5642918&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22275486%26dopt%3DAbstract</link>
            <description>Conclusions:Hyperamylinemia promotes amylin deposition in the heart, causing alterations of cardiac myocyte structure and function. We propose that detection and disruption of cardiac amylin buildup may be both a predictor of heart dysfunction and a novel therapeutic strategy in diabetic cardiomyopathy.
    PMID: 22275486 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5642918</comments>
            <pubDate>Tue, 24 Jan 2012 05:00:00 +0100</pubDate>
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        <item>
            <title>Cardiomyogenesis in the Developing Heart Is Regulated by C-Kit-Positive Cardiac Stem Cells.</title>
            <link>http://www.medworm.com/index.php?rid=5642917&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22275487%26dopt%3DAbstract</link>
            <description>Conclusions:Myocyte formation derived from CSC differentiation is the major determinant of cardiac growth during development. Division of c-kit-positive CSCs in the mouse is promoted by spontaneous Ca(2+) spikes, which dictate the pattern of stem cell replication and the generation of a myocyte progeny at all phases of prenatal life and up to one day after birth.
    PMID: 22275487 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5642917</comments>
            <pubDate>Tue, 24 Jan 2012 05:00:00 +0100</pubDate>
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        <item>
            <title>Reprogrammed endothelial cells: cell therapy for coronary collateral growth?</title>
            <link>http://www.medworm.com/index.php?rid=5624969&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22267835%26dopt%3DAbstract</link>
            <description>Authors: Faber JE
    PMID: 22267835 [PubMed - in process] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5624969</comments>
            <pubDate>Fri, 20 Jan 2012 05:00:00 +0100</pubDate>
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        <item>
            <title>Novel avenues for cell therapy in acute myocardial infarction.</title>
            <link>http://www.medworm.com/index.php?rid=5624968&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22267836%26dopt%3DAbstract</link>
            <description>Authors: Leistner DM, Zeiher AM
    PMID: 22267836 [PubMed - in process] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5624968</comments>
            <pubDate>Fri, 20 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5624968</guid>        </item>
        <item>
            <title>Weighing in on Heart Failure: The Role of SERCA2a SUMOylation.</title>
            <link>http://www.medworm.com/index.php?rid=5624967&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22267837%26dopt%3DAbstract</link>
            <description>Authors: Schwartz RJ, Yeh ET
    PMID: 22267837 [PubMed - in process] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5624967</comments>
            <pubDate>Fri, 20 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5624967</guid>        </item>
        <item>
            <title>Development, maturation, and transdifferentiation of cardiac sympathetic nerves.</title>
            <link>http://www.medworm.com/index.php?rid=5624966&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22267838%26dopt%3DAbstract</link>
            <description>We reported that cardiac sympathetic rejuvenation occurs in cardiac hypertrophy and, moreover, interleukin-6 cytokines secreted from the failing myocardium induce cholinergic transdifferentiation of the cardiac sympathetic system via a gp130 signaling pathway, affecting cardiac performance and prognosis. In this review, we summarize the molecular mechanisms involved in sympathetic development, maturation, and transdifferentiation, and propose their investigation as new therapeutic targets for heart disease.
    PMID: 22267838 [PubMed - in process] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5624966</comments>
            <pubDate>Fri, 20 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5624966</guid>        </item>
        <item>
            <title>Genetic basis of atherosclerosis: insights from mice and humans.</title>
            <link>http://www.medworm.com/index.php?rid=5624965&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22267839%26dopt%3DAbstract</link>
            <description>Authors: Stylianou IM, Bauer RC, Reilly MP, Rader DJ
    Abstract
    Atherosclerosis is a complex and heritable disease involving multiple cell types and the interactions of many different molecular pathways. The genetic and molecular mechanisms of atherosclerosis have, in part, been elucidated by mouse models; at least 100 different genes have been shown to influence atherosclerosis in mice. Importantly, unbiased genome-wide association studies have recently identified a number of novel loci robustly associated with atherosclerotic coronary artery disease. Here, we review the genetic data elucidated from mouse models of atherosclerosis, as well as significant associations for human coronary artery disease. Furthermore, we discuss in greater detail some of these novel human coronary arter...</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5624965</comments>
            <pubDate>Fri, 20 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5624965</guid>        </item>
        <item>
            <title>Leukocyte-derived microparticles in vascular homeostasis.</title>
            <link>http://www.medworm.com/index.php?rid=5624964&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22267840%26dopt%3DAbstract</link>
            <description>Authors: Angelillo-Scherrer A
    Abstract
    Leukocyte-derived microparticles (LMPs) may originate from neutrophils, monocytes/macrophages, and lymphocytes. They express markers from their parental cells and harbor membrane and cytoplasmic proteins as well as bioactive lipids implicated in a variety of mechanisms, maintaining or disrupting vascular homeostasis. When they carry tissue factor or coagulation inhibitors, they participate in hemostasis and pathological thrombosis. Both proinflammatory and anti-inflammatory processes can be affected by LMPs, thus ensuring an appropriate inflammatory response. LMPs also play a dual role in the endothelium by either improving the endothelial function or inducing an endothelial dysfunction. LMPs are implicated in all stages of atherosclerosis. Th...</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5624964</comments>
            <pubDate>Fri, 20 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5624964</guid>        </item>
        <item>
            <title>P90RSK Targets the ERK5-CHIP Ubiquitin E3 Ligase Activity in Diabetic Hearts and Promotes Cardiac Apoptosis and Dysfunction.</title>
            <link>http://www.medworm.com/index.php?rid=5624963&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22267842%26dopt%3DAbstract</link>
            <description>Conclusions:These data suggest a role for p90RSK in inhibiting CHIP activity and promoting cardiac apoptosis through binding to and phosphorylation of ERK5-S496.
    PMID: 22267842 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5624963</comments>
            <pubDate>Thu, 19 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5624963</guid>        </item>
        <item>
            <title>Thioredoxin Interacting Protein Promotes Endothelial Cell Inflammation in Response to Disturbed Flow by Increasing Leukocyte Adhesion and Repressing Kruppel-Like Factor 2.</title>
            <link>http://www.medworm.com/index.php?rid=5624962&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22267843%26dopt%3DAbstract</link>
            <description>Conclusions:These data demonstrate the essential role for TXNIP in mediating EC-leukocyte adhesion under d-flow, as well as define a novel mechanism by which TXNIP acts as a transcriptional corepressor to regulate Kruppel-like factor 2-dependent gene expression.
    PMID: 22267843 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5624962</comments>
            <pubDate>Thu, 19 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5624962</guid>        </item>
        <item>
            <title>Subcellular Structures and Function of Myocytes Impaired During Heart Failure Are Restored by Cardiac Resynchronization Therapy.</title>
            <link>http://www.medworm.com/index.php?rid=5624970&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22253411%26dopt%3DAbstract</link>
            <description>Conclusions:DHF is associated with regional remodeling of the t-system. Myocytes undergo substantial structural and functional restoration after only 3 weeks of CRT. The finding suggests that t-system status can provide an early marker of the success of this therapy. The results could also guide us to an understanding of the loss and remodeling of proteins associated with the t-system. The steep relationship between free Ca(2+) and contraction suggests that some restoration of Ca(2+) release units will have a disproportionately large effect on contractility.
    PMID: 22253411 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5624970</comments>
            <pubDate>Tue, 17 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5624970</guid>        </item>
        <item>
            <title>Bmp Signaling Exerts Opposite Effects on Cardiac Differentiation.</title>
            <link>http://www.medworm.com/index.php?rid=5604965&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22247485%26dopt%3DAbstract</link>
            <description>Conclusions:Bmp signaling exerts opposing effects on myocardial differentiation in the embryo by promoting as well as inhibiting cardiac growth.
    PMID: 22247485 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5604965</comments>
            <pubDate>Thu, 12 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5604965</guid>        </item>
        <item>
            <title>Editorial board.</title>
            <link>http://www.medworm.com/index.php?rid=5579022&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22223203%26dopt%3DAbstract</link>
            <description>Authors: 
    PMID: 22223203 [PubMed - in process] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5579022</comments>
            <pubDate>Fri, 06 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5579022</guid>        </item>
        <item>
            <title>Fetal cell microchimerism in the maternal heart: baby gives back.</title>
            <link>http://www.medworm.com/index.php?rid=5579021&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22223204%26dopt%3DAbstract</link>
            <description>Authors: Pritchard S, Bianchi DW
    PMID: 22223204 [PubMed - in process] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5579021</comments>
            <pubDate>Fri, 06 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5579021</guid>        </item>
        <item>
            <title>On circadian variation of myocardial reperfusion injury.</title>
            <link>http://www.medworm.com/index.php?rid=5579020&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22223205%26dopt%3DAbstract</link>
            <description>Authors: Braunwald E
    PMID: 22223205 [PubMed - in process] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5579020</comments>
            <pubDate>Fri, 06 Jan 2012 05:00:00 +0100</pubDate>
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        <item>
            <title>A Second Chance for a PPARγ Targeted Therapy?</title>
            <link>http://www.medworm.com/index.php?rid=5579019&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22223206%26dopt%3DAbstract</link>
            <description>Authors: Norris AW, Sigmund CD
    PMID: 22223206 [PubMed - in process] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5579019</comments>
            <pubDate>Fri, 06 Jan 2012 05:00:00 +0100</pubDate>
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        <item>
            <title>Impact through discovery: a global challenge: presidential address at the american heart association 2011 scientific sessions.</title>
            <link>http://www.medworm.com/index.php?rid=5579018&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22223207%26dopt%3DAbstract</link>
            <description>Authors: Tomaselli GF
    PMID: 22223207 [PubMed - in process] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5579018</comments>
            <pubDate>Fri, 06 Jan 2012 05:00:00 +0100</pubDate>
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        <item>
            <title>Thrombin receptor activation work wins 2011 lucian award.</title>
            <link>http://www.medworm.com/index.php?rid=5579017&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22223208%26dopt%3DAbstract</link>
            <description>Authors: McCarthy A
    PMID: 22223208 [PubMed - in process] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5579017</comments>
            <pubDate>Fri, 06 Jan 2012 05:00:00 +0100</pubDate>
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        <item>
            <title>The fire within: cardiac inflammatory signaling in health and disease.</title>
            <link>http://www.medworm.com/index.php?rid=5579016&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22223209%26dopt%3DAbstract</link>
            <description>Authors: Coggins M, Rosenzweig A
    Abstract
    Inflammatory mediators are operative in the pathogenesis of the most common forms of heart disease. Although in most cases the induction of these pathways is maladaptive and deleterious, there are notable exceptions when inflammatory pathways participate in healing or limiting the extent of injury. The appreciation of the role of these mechanisms in myocardial homeostasis and pathophysiology has led to increased efforts to elucidate the specific signaling pathways most relevant to the heart. Our goal in this introductory overview is to provide context for the five detailed reviews that follow by introducing the major relevant stimuli, the receptors, and pathways that mediate inflammatory signaling in the heart. We try to impart a sense of t...</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5579016</comments>
            <pubDate>Fri, 06 Jan 2012 05:00:00 +0100</pubDate>
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        <item>
            <title>Inflammation in myocardial diseases.</title>
            <link>http://www.medworm.com/index.php?rid=5579015&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22223210%26dopt%3DAbstract</link>
            <description>Authors: Marchant DJ, Boyd JH, Lin DC, Granville DJ, Garmaroudi FS, McManus BM
    Abstract
    Inflammatory processes underlie a broad spectrum of conditions that injure the heart muscle and cause both structural and functional deficits. In this article, we address current knowledge regarding 4 common forms of myocardial inflammation: myocardial ischemia and reperfusion, sepsis, viral myocarditis, and immune rejection. Each of these pathological states has its own unique features in pathogenesis and disease evolution, but all reflect inflammatory mechanisms that are partially shared. From the point of injury to the mobilization of innate and adaptive immune responses and inflammatory amplification, the cellular and soluble mediators and mechanisms examined in this review will be discussed...</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5579015</comments>
            <pubDate>Fri, 06 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5579015</guid>        </item>
        <item>
            <title>Autoantibodies in heart failure and cardiac dysfunction.</title>
            <link>http://www.medworm.com/index.php?rid=5579014&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22223211%26dopt%3DAbstract</link>
            <description>Authors: Kaya Z, Leib C, Katus HA
    Abstract
    Human heart failure is a disease with multifactorial causes, considerable morbidity, and high mortality. Several circulating autoantibodies, some of them being heart-specific, play a crucial role in the progression and induction of heart failure. However the precise mechanisms on how these autoantibodies perpetuate or even induce an organ specific autoimmune response are not yet fully understood. Also it is being a matter of current research to elucidate a potential pathophysiological role of the innate immune system in generating auto-reactive antibodies. In this review we will summarize the current available literature on circulating autoantibodies which are related to human heart failure. We will present clinical and animal studies that...</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5579014</comments>
            <pubDate>Fri, 06 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5579014</guid>        </item>
        <item>
            <title>Regulation of the inflammatory response in cardiac repair.</title>
            <link>http://www.medworm.com/index.php?rid=5579013&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22223212%26dopt%3DAbstract</link>
            <description>Authors: Frangogiannis NG
    Abstract
    Myocardial necrosis triggers an inflammatory reaction that clears the wound from dead cells and matrix debris, while activating reparative pathways necessary for scar formation. A growing body of evidence suggests that accentuation, prolongation, or expansion of the postinfarction inflammatory response results in worse remodeling and dysfunction following myocardial infarction. This review manuscript discusses the cellular effectors and endogenous molecular signals implicated in suppression and containment of the inflammatory response in the infarcted heart. Clearance of apoptotic neutrophils, recruitment of inhibitory monocyte subsets and regulatory T cells, macrophage differentiation and pericyte/endothelial interactions may play an active role ...</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5579013</comments>
            <pubDate>Fri, 06 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5579013</guid>        </item>
        <item>
            <title>Inflammation, Endoplasmic Reticulum Stress, Autophagy, and the Monocyte Chemoattractant Protein-1/CCR2 Pathway.</title>
            <link>http://www.medworm.com/index.php?rid=5579012&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22223213%26dopt%3DAbstract</link>
            <description>Authors: Kolattukudy PE, Niu J
    Abstract
    Numerous inflammatory cytokines have been implicated in the pathogenesis of cardiovascular diseases. Monocyte chemoattractant protein (MCP)-1/CCL2 is expressed by mainly inflammatory cells and stromal cells such as endothelial cells, and its expression is upregulated after proinflammatory stimuli and tissue injury. MCP-1 can function as a traditional chemotactic cytokine and also regulates gene transcription. The recently discovered novel zinc-finger protein, called MCPIP (MCP-1-induced protein), initiates a series of signaling events that causes oxidative and endoplasmic reticulum (ER) stress, leading to autophagy that can result in cell death or differentiation, depending on the cellular context. After a brief review of the basic processes ...</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5579012</comments>
            <pubDate>Fri, 06 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5579012</guid>        </item>
        <item>
            <title>Hydrogen sulfide as an endothelium-derived hyperpolarizing factor in rodent mesenteric arteries.</title>
            <link>http://www.medworm.com/index.php?rid=5579011&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22223214%26dopt%3DAbstract</link>
            <description>Authors: Edwards G, Félétou M, Weston AH
    PMID: 22223214 [PubMed - in process] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5579011</comments>
            <pubDate>Fri, 06 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5579011</guid>        </item>
        <item>
            <title>Cardiomyocyte renewal in humans.</title>
            <link>http://www.medworm.com/index.php?rid=5579010&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22223215%26dopt%3DAbstract</link>
            <description>Authors: Bergmann O, Zdunek S, Frisén J, Bernard S, Druid H, Jovinge S
    PMID: 22223215 [PubMed - in process] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5579010</comments>
            <pubDate>Fri, 06 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5579010</guid>        </item>
        <item>
            <title>Shortened Ca2+ Signaling Refractoriness Underlies Cellular Arrhythmogenesis in a Postinfarction Model of Sudden Cardiac Death.</title>
            <link>http://www.medworm.com/index.php?rid=5579009&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22223353%26dopt%3DAbstract</link>
            <description>Conclusions:The attainment of a certain threshold [Ca(2+)](SR) is not sufficient for the generation of DCWs. Postrelease Ca(2+) signaling refractoriness critically influences the occurrence of spontaneous Ca(2+) waves in the diastolic period. Shortened Ca(2+) signaling refractoriness due to RyR2 phosphorylation and oxidation is responsible for the increased rate of DCWs observed in VF myocytes.
    PMID: 22223353 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5579009</comments>
            <pubDate>Thu, 05 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5579009</guid>        </item>
        <item>
            <title>Endosomal Actin Remodeling by Coronin-1A Controls Lipoprotein Uptake and Degradation in Macrophages.</title>
            <link>http://www.medworm.com/index.php?rid=5579008&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22223354%26dopt%3DAbstract</link>
            <description>Conclusions:Coro1A controls actin association with endocytic organelles, thereby negatively regulating endo-lysosomal delivery, degradation of modified lipoproteins and cholesterol deposition in macrophages.
    PMID: 22223354 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5579008</comments>
            <pubDate>Thu, 05 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5579008</guid>        </item>
        <item>
            <title>Left-Right Symmetry Breaking in Tissue Morphogenesis via Cytoskeletal Mechanics.</title>
            <link>http://www.medworm.com/index.php?rid=5579007&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22223355%26dopt%3DAbstract</link>
            <description>Conclusions:Our results show that adult stem cells retain inherent LR asymmetry that elicits de novo macroscale tissue morphogenesis, indicating that mechanical induction is required for cellular LR specification.
    PMID: 22223355 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5579007</comments>
            <pubDate>Thu, 05 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5579007</guid>        </item>
        <item>
            <title>High-Mobility Group A1 Protein: A New Coregulator of Peroxisome Proliferator-Activated Receptor-γ-Mediated Transrepression in the Vasculature.</title>
            <link>http://www.medworm.com/index.php?rid=5562796&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22207709%26dopt%3DAbstract</link>
            <description>Conclusions:The present data suggest that ligand-dependent formation of HMGA1-Ubc9-PPARγ complexes facilitates PPARγ SUMOylation, which results in the prevention of SMRT corepressor clearance and induction of MMP-9 transrepression. These data provide new information on PPARγ-dependent vascular transcriptional regulation and help us to understand the molecular consequences of therapeutic interventions with PPARγ ligands in the vasculature.
    PMID: 22207709 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5562796</comments>
            <pubDate>Thu, 29 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5562796</guid>        </item>
        <item>
            <title>FRS2α-Mediated FGF Signals Suppress Premature Differentiation of Cardiac Stem Cells Through Regulating Autophagy Activity.</title>
            <link>http://www.medworm.com/index.php?rid=5562795&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22207710%26dopt%3DAbstract</link>
            <description>Conclusions:The results indicate that the FGF/FRS2α-mediated signals prevent premature differentiation of heart progenitor cells through suppressing autophagy. The findings provide the first evidence that autophagy plays a role in heart progenitor differentiation.
    PMID: 22207710 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5562795</comments>
            <pubDate>Thu, 29 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5562795</guid>        </item>
        <item>
            <title>Inhalation of Nitric Oxide Prevents Ischemic Brain Damage in Experimental Stroke by Selective Dilatation of Collateral Arterioles.</title>
            <link>http://www.medworm.com/index.php?rid=5562794&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22207711%26dopt%3DAbstract</link>
            <description>Conclusions:Inhaled nitric oxide thus may provide a completely novel strategy to improve penumbral blood flow and neuronal survival in stroke or other ischemic conditions.
    PMID: 22207711 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5562794</comments>
            <pubDate>Thu, 29 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5562794</guid>        </item>
        <item>
            <title>Vascular Bioactivation of Nitroglycerin Is Catalyzed by Cytosolic Aldehyde Dehydrogenase-2.</title>
            <link>http://www.medworm.com/index.php?rid=5562793&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22207712%26dopt%3DAbstract</link>
            <description>Conclusions:The data indicate that vascular bioactivation of GTN is catalyzed by cytosolic ALDH2. Mitochondrial GTN metabolism may contribute to oxidative stress-related adverse effects of nitrate therapy and the development of nitrate tolerance.
    PMID: 22207712 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5562793</comments>
            <pubDate>Thu, 29 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5562793</guid>        </item>
        <item>
            <title>NR4A1 (Nur77) Deletion Polarizes Macrophages Toward an Inflammatory Phenotype and Increases Atherosclerosis.</title>
            <link>http://www.medworm.com/index.php?rid=5536887&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22194622%26dopt%3DAbstract</link>
            <description>Conclusions:We conclude that the absence of Nur77 in monocytes and macrophages results in enhanced toll-like receptor signaling and polarization of macrophages toward a proinflammatory M1 phenotype. Despite having fewer monocytes, Nur77(-/-) mice developed significant atherosclerosis when fed a Western diet. These studies indicate that Nur77 is a novel target for modulating the inflammatory phenotype of monocytes and macrophages and may be important for regulation of atherogenesis.
    PMID: 22194622 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5536887</comments>
            <pubDate>Thu, 22 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5536887</guid>        </item>
        <item>
            <title>Bone Marrow-Specific Deficiency of Nuclear Receptor Nur77 Enhances Atherosclerosis.</title>
            <link>http://www.medworm.com/index.php?rid=5536886&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22194623%26dopt%3DAbstract</link>
            <description>Conclusions:In conclusion, in bone marrow-derived cells the nuclear receptor Nur77 has an anti-inflammatory function, represses SDF-1α expression and inhibits atherosclerosis.
    PMID: 22194623 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5536886</comments>
            <pubDate>Thu, 22 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5536886</guid>        </item>
        <item>
            <title>Integrin-Linked Kinase Regulates Vasomotor Function by Preventing Endothelial Nitric Oxide Synthase Uncoupling: Role in Atherosclerosis.</title>
            <link>http://www.medworm.com/index.php?rid=5536885&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22194624%26dopt%3DAbstract</link>
            <description>Conclusions:Our results identify ILK as a regulatory partner of eNOS in vivo that prevents eNOS uncoupling, and suggest ILK as a therapeutic target for prevention of endothelial dysfunction related to shear stress-induced vascular diseases.
    PMID: 22194624 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5536885</comments>
            <pubDate>Thu, 22 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5536885</guid>        </item>
        <item>
            <title>The Role of Fibroblasts in Complex Fractionated Electrograms During Persistent/Permanent Atrial Fibrillation: Implications for Electrogram-Based Catheter Ablation.</title>
            <link>http://www.medworm.com/index.php?rid=5536889&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22179057%26dopt%3DAbstract</link>
            <description>Conclusions:Fibroblast proliferation in atria might be responsible for the genesis of CFAEs during persistent/permanent AF. Our findings could contribute to better understanding of the mechanisms underlying CFAE-targeted AF ablation.
    PMID: 22179057 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5536889</comments>
            <pubDate>Wed, 21 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5536889</guid>        </item>
        <item>
            <title>Gi-Biased β2AR Signaling Links GRK2 Upregulation to Heart Failure.</title>
            <link>http://www.medworm.com/index.php?rid=5536888&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22179058%26dopt%3DAbstract</link>
            <description>Conclusions:Our data show that enhanced β(2)AR phosphorylation by GRK, in addition to PKA, leads the receptor to G(i)-biased signaling, which, in turn, contributes to the pathogenesis of heart failure, marking G(i)-biased β(2)AR signaling as a primary event linking upregulation of GRK to cardiac maladaptive remodeling, failure and cardiodepression.
    PMID: 22179058 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5536888</comments>
            <pubDate>Wed, 21 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5536888</guid>        </item>
        <item>
            <title>PKC-ing Is Believing: Targeting Protein Kinase C in Heart Failure.</title>
            <link>http://www.medworm.com/index.php?rid=5514769&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22158646%26dopt%3DAbstract</link>
            <description>Authors: Belmonte SL, Blaxall BC
    PMID: 22158646 [PubMed - in process] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5514769</comments>
            <pubDate>Fri, 09 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5514769</guid>        </item>
        <item>
            <title>Mitochondrial Angiotensin receptors and aging.</title>
            <link>http://www.medworm.com/index.php?rid=5514768&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22158647%26dopt%3DAbstract</link>
            <description>Authors: Inagami T
    PMID: 22158647 [PubMed - in process] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5514768</comments>
            <pubDate>Fri, 09 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5514768</guid>        </item>
        <item>
            <title>Elizabeth McNally: Taking on Inherited Cardiovascular Disorders.</title>
            <link>http://www.medworm.com/index.php?rid=5514767&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22158648%26dopt%3DAbstract</link>
            <description>Authors: McCarthy A
    PMID: 22158648 [PubMed - in process] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5514767</comments>
            <pubDate>Fri, 09 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5514767</guid>        </item>
        <item>
            <title>Empowering adult stem cells for myocardial regeneration.</title>
            <link>http://www.medworm.com/index.php?rid=5514766&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22158649%26dopt%3DAbstract</link>
            <description>Authors: Mohsin S, Siddiqi S, Collins B, Sussman MA
    Abstract
    Treatment strategies for heart failure remain a high priority for ongoing research due to the profound unmet need in clinical disease coupled with lack of significant translational progress. The underlying issue is the same whether the cause is acute damage, chronic stress from disease, or aging: progressive loss of functional cardiomyocytes and diminished hemodynamic output. To stave off cardiomyocyte losses, a number of strategic approaches have been embraced in recent years involving both molecular and cellular approaches to augment myocardial structure and performance. Resultant excitement surrounding regenerative medicine in the heart has been tempered by realizations that reparative processes in the heart are insuff...</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5514766</comments>
            <pubDate>Fri, 09 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5514766</guid>        </item>
        <item>
            <title>Signaling during epicardium and coronary vessel development.</title>
            <link>http://www.medworm.com/index.php?rid=5514765&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22158650%26dopt%3DAbstract</link>
            <description>Authors: Pérez-Pomares JM, de la Pompa JL
    Abstract
    The epicardium, the tissue layer covering the cardiac muscle (myocardium), develops from the proepicardium, a mass of coelomic progenitors located at the venous pole of the embryonic heart. Proepicardium cells attach to and spread over the myocardium to form the primitive epicardial epithelium. The epicardium subsequently undergoes an epithelial-to-mesenchymal transition to give rise to a population of epicardium-derived cells, which in turn invade the heart and progressively differentiate into various cell types, including cells of coronary blood vessels and cardiac interstitial cells. Epicardial cells and epicardium-derived cells signal to the adjacent cardiac muscle in a paracrine fashion, promoting its proliferation and expans...</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5514765</comments>
            <pubDate>Fri, 09 Dec 2011 05:00:00 +0100</pubDate>
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        <item>
            <title>Thymosin Beta 4 Is Dispensable for Murine Cardiac Development and Function.</title>
            <link>http://www.medworm.com/index.php?rid=5514764&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22158707%26dopt%3DAbstract</link>
            <description>Conclusions:We conclude that Tβ4 is dispensable for embryonic viability, heart development, coronary vessel development, and adult myocardial function.
    PMID: 22158707 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5514764</comments>
            <pubDate>Thu, 08 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5514764</guid>        </item>
        <item>
            <title>Polycomb Repressive Complex 2 Regulates Normal Development of the Mouse Heart.</title>
            <link>http://www.medworm.com/index.php?rid=5514763&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22158708%26dopt%3DAbstract</link>
            <description>Conclusions:Our study reveals a previously undescribed role of EZH2 in regulating heart formation and shows that perturbation of the epigenetic landscape early in cardiogenesis has sustained disruptive effects at later developmental stages.
    PMID: 22158708 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5514763</comments>
            <pubDate>Thu, 08 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5514763</guid>        </item>
        <item>
            <title>Inhibition of CaMKII Phosphorylation of RyR2 Prevents Induction of Atrial Fibrillation in FKBP12.6 Knockout Mice.</title>
            <link>http://www.medworm.com/index.php?rid=5514762&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22158709%26dopt%3DAbstract</link>
            <description>Conclusions:FKBP12.6 mice exhibit AF caused by SR Ca(2+) leak, Na(+)/Ca(2+)-exchanger activation, and DADs, which promote triggered activity. Genetic inhibition of RyR2-S2814 phosphorylation prevents AF induction in FKBP12.6-/- mice by suppressing SR Ca(2+) leak and DADs. These results suggest suppression of RyR2-S2814 phosphorylation as a potential anti-AF therapeutic target.
    PMID: 22158709 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5514762</comments>
            <pubDate>Thu, 08 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5514762</guid>        </item>
        <item>
            <title>H2O2-Induced Dilation in Human Coronary Arterioles: Role of Protein Kinase G Dimerization and Large-Conductance Ca2+-Activated K+ Channel Activation.</title>
            <link>http://www.medworm.com/index.php?rid=5514761&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22158710%26dopt%3DAbstract</link>
            <description>Conclusions:H(2)O(2) dilates HCAs through a novel mechanism involving protein dimerization and activation of PKG-Iα and subsequent opening of smooth muscle BK(Ca) channels.
    PMID: 22158710 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5514761</comments>
            <pubDate>Thu, 08 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5514761</guid>        </item>
        <item>
            <title>Etsrp/Etv2 Is Directly Regulated by Foxc1a/b in the Zebrafish Angioblast.</title>
            <link>http://www.medworm.com/index.php?rid=5514770&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22135404%26dopt%3DAbstract</link>
            <description>Conclusions:These findings identify mesodermal foxc1a/b as a direct upstream regulator of etsrp in angioblasts. This establishes a new molecular link in the process of mesoderm specification into angioblast.
    PMID: 22135404 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5514770</comments>
            <pubDate>Thu, 01 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5514770</guid>        </item>
        <item>
            <title>FSP-1 Silencing in Bone Marrow Cells Suppresses Neointima Formation in Vein Graft.</title>
            <link>http://www.medworm.com/index.php?rid=5514775&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22116816%26dopt%3DAbstract</link>
            <description>Conclusions:BM-derived FSP-1(+) cells enhance neointima formation through an increase in transendothelial invasion with stimulation of SMC proliferation. The Rac1 and ERK5 signaling cascade mediate FSP-1-induced responses in SMCs and BM cells. This novel pathophysiology suggests a new therapeutic target, FSP-1, for preventing the development of neointima in vein grafts.
    PMID: 22116816 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5514775</comments>
            <pubDate>Wed, 23 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5514775</guid>        </item>
        <item>
            <title>STAT5 Activation and Cardioprotection by Remote Ischemic Preconditioning in Humans.</title>
            <link>http://www.medworm.com/index.php?rid=5514774&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22116817%26dopt%3DAbstract</link>
            <description>Conclusions:The identification of this unique signaling signature of RIPC will facilitate the development of pharmacological cardioprotection.Clinical Trial Registration:URL: http://www.clinicaltrials.gov. Unique identifier: NCT01406678.
    PMID: 22116817 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5514774</comments>
            <pubDate>Wed, 23 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5514774</guid>        </item>
        <item>
            <title>Regulated Expression and Role of c-Myb in the Cardiovascular-Directed Differentiation of Mouse Embryonic Stem Cells.</title>
            <link>http://www.medworm.com/index.php?rid=5514773&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22116818%26dopt%3DAbstract</link>
            <description>Conclusions:c-Myb is tightly regulated by proteosomal degradation during cardiovascular-directed differentiation of ESC, expanding early-stage VEGFR2+ progenitors capable of retinoic acid-responsive SMC formation.
    PMID: 22116818 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5514773</comments>
            <pubDate>Wed, 23 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5514773</guid>        </item>
        <item>
            <title>miR-29b Participates in Early Aneurysm Development in Marfan Syndrome.</title>
            <link>http://www.medworm.com/index.php?rid=5514772&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22116819%26dopt%3DAbstract</link>
            <description>Conclusions:We identify increased miR-29b expression as key to the pathogenesis of early aneurysm development in MFS by regulating aortic wall apoptosis and extracellular matrix abnormalities.
    PMID: 22116819 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5514772</comments>
            <pubDate>Wed, 23 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5514772</guid>        </item>
        <item>
            <title>Selective Modulation of Nuclear Factor of Activated T-Cell Function in Restenosis by a Potent Bipartite Peptide Inhibitor.</title>
            <link>http://www.medworm.com/index.php?rid=5514771&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22116820%26dopt%3DAbstract</link>
            <description>Conclusions:We designed a bipartite NFAT inhibitor that is more potent than VIVIT and more selective than CsA. MCV1 constitutes not only a powerful tool to unravel NFAT function but also a potential drug candidate for the treatment of diseases implicating NFAT activation.
    PMID: 22116820 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5514771</comments>
            <pubDate>Wed, 23 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5514771</guid>        </item>
        <item>
            <title>Pressure-Overload-Induced Subcellular Relocalization/Oxidation of Soluble Guanylate Cyclase in the Heart Modulates Enzyme Stimulation.</title>
            <link>http://www.medworm.com/index.php?rid=5424037&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22095726%26dopt%3DAbstract</link>
            <description>Conclusions:Pressure overload depresses NO/heme-dependent sGC activation in the heart, consistent with enhanced oxidation. The data reveal a novel additional mechanism for reduced NO-coupled sGC activity related to dynamic shifts in membrane microdomain localization, with Cav3-microdomains protecting sGC from heme-oxidation and facilitating NO responsiveness. Translocation of sGC out of this domain favors sGC oxidation and contributes to depressed NO-stimulated sGC activity.
    PMID: 22095726 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5424037</comments>
            <pubDate>Thu, 17 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5424037</guid>        </item>
        <item>
            <title>Circadian Dependence of Infarct Size and Left Ventricular Function After ST Elevation Myocardial Infarction.</title>
            <link>http://www.medworm.com/index.php?rid=5424036&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22095727%26dopt%3DAbstract</link>
            <description>Conclusions:The results of this study demonstrate for the first time in humans that myocardial infarct size and left ventricular function after STEMI have a circadian dependence on the time of day onset of ischemia.
    PMID: 22095727 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5424036</comments>
            <pubDate>Thu, 17 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5424036</guid>        </item>
        <item>
            <title>Acidosis Dilates Brain Parenchymal Arterioles by Conversion of Calcium Waves to Sparks to Activate BK Channels.</title>
            <link>http://www.medworm.com/index.php?rid=5424035&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22095728%26dopt%3DAbstract</link>
            <description>Conclusions:These results support the novel concept that acidification, by converting Ca(2+) waves to sparks, leads to the activation of BK(Ca) channels to induce dilation of cerebral PAs.
    PMID: 22095728 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5424035</comments>
            <pubDate>Thu, 17 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5424035</guid>        </item>
        <item>
            <title>Induction of Vascular Progenitor Cells From Endothelial Cells Stimulates Coronary Collateral Growth.</title>
            <link>http://www.medworm.com/index.php?rid=5424034&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22095729%26dopt%3DAbstract</link>
            <description>Conclusions:We conclude that iVPCs, generated by partially reprogramming ECs, are an ideal cell type for cell-based therapy designed to stimulate coronary collateral growth.
    PMID: 22095729 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5424034</comments>
            <pubDate>Thu, 17 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5424034</guid>        </item>
        <item>
            <title>Dominant-Negative Control of cAMP-Dependent IKs Upregulation in Human Long-QT Syndrome Type 1.</title>
            <link>http://www.medworm.com/index.php?rid=5424033&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22095730%26dopt%3DAbstract</link>
            <description>Conclusions:Our results indicate the involvement of the KCNQ1-S6 region at/or around A341 in cAMP-dependent stimulation of I(Ks), a process that is under strong dominant-negative control, suggesting that tetrameric KCNQ1 phosphorylation is required. Specific long-QT1 mutations, including heterozygous A341V, disable this regulation.
    PMID: 22095730 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5424033</comments>
            <pubDate>Thu, 17 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5424033</guid>        </item>
        <item>
            <title>Fetal Cells Traffic to Injured Maternal Myocardium and Undergo Cardiac Differentiation.</title>
            <link>http://www.medworm.com/index.php?rid=5424038&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22082491%26dopt%3DAbstract</link>
            <description>Conclusions:Fetal maternal stem cell transfer appears to be a critical mechanism in the maternal response to cardiac injury. Furthermore, we have identified Cdx2 cells as a novel cell type for potential use in cardiovascular regenerative therapy.
    PMID: 22082491 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5424038</comments>
            <pubDate>Mon, 14 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5424038</guid>        </item>
        <item>
            <title>Blunting half of the double-edged sword: potential use of interleukin-10 to protect bone marrow-derived cells after myocardial infarction.</title>
            <link>http://www.medworm.com/index.php?rid=5424048&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22076503%26dopt%3DAbstract</link>
            <description>Authors: Springer ML, Wang X
    PMID: 22076503 [PubMed - in process] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5424048</comments>
            <pubDate>Fri, 11 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5424048</guid>        </item>
        <item>
            <title>Opening the field of integrin biology to &quot;biased agonism&quot;.</title>
            <link>http://www.medworm.com/index.php?rid=5424047&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22076504%26dopt%3DAbstract</link>
            <description>Opening the field of integrin biology to &quot;biased agonism&quot;.
    Circ Res. 2011 Nov 11;109(11):1199-201
    Authors: Simon DI
    PMID: 22076504 [PubMed - in process] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5424047</comments>
            <pubDate>Fri, 11 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5424047</guid>        </item>
        <item>
            <title>Widespread promiscuous genetic information transfer from DNA to RNA.</title>
            <link>http://www.medworm.com/index.php?rid=5424046&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22076505%26dopt%3DAbstract</link>
            <description>Authors: Chakravarti A
    PMID: 22076505 [PubMed - in process] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5424046</comments>
            <pubDate>Fri, 11 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5424046</guid>        </item>
        <item>
            <title>Meeting report for basic cardiovascular sciences 2011 scientific sessions: from concept to clinic: leading cardiovascular translational science.</title>
            <link>http://www.medworm.com/index.php?rid=5424045&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22076506%26dopt%3DAbstract</link>
            <description>Authors: Sadoshima J, Hare JM
    PMID: 22076506 [PubMed - in process] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5424045</comments>
            <pubDate>Fri, 11 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5424045</guid>        </item>
        <item>
            <title>Grown Up Mice From Gene-Corrected iPS Cells.</title>
            <link>http://www.medworm.com/index.php?rid=5424044&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22076507%26dopt%3DAbstract</link>
            <description>Authors: Laidman J
    PMID: 22076507 [PubMed - in process] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5424044</comments>
            <pubDate>Fri, 11 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5424044</guid>        </item>
        <item>
            <title>Late-Breaking Basic Science Abstracts From the American Heart Association's Scientific Sessions 2011.</title>
            <link>http://www.medworm.com/index.php?rid=5424039&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22080354%26dopt%3DAbstract</link>
            <description>Authors: 
    PMID: 22080354 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5424039</comments>
            <pubDate>Fri, 11 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5424039</guid>        </item>
        <item>
            <title>Adrenergic Signaling Controls RGK-Dependent Trafficking of Cardiac Voltage-Gated L-Type Ca2+ Channels Through PKD1.</title>
            <link>http://www.medworm.com/index.php?rid=5424043&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22076634%26dopt%3DAbstract</link>
            <description>Conclusion:The α(1)-adrenergic stimulation releases Rem1 inhibition of VLCCs through direct phosphorylation of Rem1 at Ser18 by protein kinase D1, resulting in an increase of the channel activity and transverse-tubule expression. Our results uncover a novel molecular regulatory mechanism of VLCC trafficking and function in the heart and provide the first demonstration of physiological regulation of RGK function.
    PMID: 22076634 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5424043</comments>
            <pubDate>Thu, 10 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5424043</guid>        </item>
        <item>
            <title>Frizzled 4 Regulates Arterial Network Organization Through Noncanonical Wnt/Planar Cell Polarity Signaling.</title>
            <link>http://www.medworm.com/index.php?rid=5424042&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22076635%26dopt%3DAbstract</link>
            <description>Conclusions:These results suggest that Fzd4 is a major receptor involved in arterial formation and organization through a Wnt/PCP pathway.
    PMID: 22076635 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5424042</comments>
            <pubDate>Thu, 10 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5424042</guid>        </item>
        <item>
            <title>Integration of Repulsive Guidance Cues Generates Avascular Zones That Shape Mammalian Blood Vessels.</title>
            <link>http://www.medworm.com/index.php?rid=5424041&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22076636%26dopt%3DAbstract</link>
            <description>Conclusions:These findings demonstrate that Sema3E-generated avascular zones are critical regulators of mammalian cardiovascular patterning and are the first to identify a repulsive role for the lateral plate mesoderm. Integration of multiple, and in some cases redundant, repulsive cues from various tissues is critical to patterning the first embryonic blood vessels.
    PMID: 22076636 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5424041</comments>
            <pubDate>Thu, 10 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5424041</guid>        </item>
        <item>
            <title>The Perlecan Fragment LG3 Is a Novel Regulator of Obliterative Remodeling Associated With Allograft Vascular Rejection.</title>
            <link>http://www.medworm.com/index.php?rid=5424040&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22076637%26dopt%3DAbstract</link>
            <description>Conclusion:These results indicate that LG3 is a novel regulator of obliterative vascular remodeling during rejection.
    PMID: 22076637 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5424040</comments>
            <pubDate>Thu, 10 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5424040</guid>        </item>
        <item>
            <title>Inhibition of miR-15 Protects Against Cardiac Ischemic Injury.</title>
            <link>http://www.medworm.com/index.php?rid=5382143&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22052914%26dopt%3DAbstract</link>
            <description>Conclusions:Oligonucleotide-based therapies using LNA-modified chemistries for modulating cardiac miRNAs in the setting of heart disease are efficacious and validate miR-15 as a potential therapeutic target for the manipulation of cardiac remodeling and function in the setting of ischemic injury.
    PMID: 22052914 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5382143</comments>
            <pubDate>Thu, 03 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5382143</guid>        </item>
        <item>
            <title>Activating Transcription Factor 1 Directs Mhem Atheroprotective Macrophages Through Coordinated Iron Handling and Foam Cell Protection.</title>
            <link>http://www.medworm.com/index.php?rid=5382142&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22052915%26dopt%3DAbstract</link>
            <description>Conclusions:These results show that ATF-1 mediates HO-1 induction by heme and drives macrophage adaptation to intraplaque hemorrhage. Our definition of an ATF-1-mediated pathway for linked protection from foam cell formation and oxidant stress may have therapeutic potential.
    PMID: 22052915 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5382142</comments>
            <pubDate>Thu, 03 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5382142</guid>        </item>
        <item>
            <title>Mitochondrial Fusion is Essential for Organelle Function and Cardiac Homeostasis.</title>
            <link>http://www.medworm.com/index.php?rid=5382141&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22052916%26dopt%3DAbstract</link>
            <description>Conclusions:Mitochondrial fusion in adult cardiac myocytes is necessary to maintain normal mitochondrial morphology and is essential for normal cardiac respiratory and contractile function. Interruption of mitochondrial fusion causes lethal cardiac failure at a time corresponding to 3 or 4 cycles of unopposed mitochondrial fission.
    PMID: 22052916 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5382141</comments>
            <pubDate>Thu, 03 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5382141</guid>        </item>
        <item>
            <title>Adventitial Delivery of an Allogeneic Bone Marrow-Derived Adherent Stem Cell in Acute Myocardial Infarction: Phase I Clinical Study.</title>
            <link>http://www.medworm.com/index.php?rid=5382140&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22052917%26dopt%3DAbstract</link>
            <description>Conclusions:In this study, the delivery of MultiStem to the myocardium in patients with recent STEMI was well tolerated and safe. In patients who exhibited significant myocardial damage, the delivery of ≥50 million MultiStem resulted in improved EF and stroke volume 4 months later. These findings support further development of MultiStem in patients with AMI and they validate the potential of a system for delivery of adult stem cells at any time after primary percutaneous coronary intervention.
    PMID: 22052917 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5382140</comments>
            <pubDate>Thu, 03 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5382140</guid>        </item>
        <item>
            <title>Modulating the MicroRNArchitecture of an Aging Aorta.</title>
            <link>http://www.medworm.com/index.php?rid=5382153&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22034476%26dopt%3DAbstract</link>
            <description>Authors: O'Rourke JR, Olson EN
    PMID: 22034476 [PubMed - in process] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5382153</comments>
            <pubDate>Fri, 28 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5382153</guid>        </item>
        <item>
            <title>Tension in the plaque: hypoxia modulates metabolism in atheroma.</title>
            <link>http://www.medworm.com/index.php?rid=5382152&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22034477%26dopt%3DAbstract</link>
            <description>Authors: Libby P, Folco E
    PMID: 22034477 [PubMed - in process] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5382152</comments>
            <pubDate>Fri, 28 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5382152</guid>        </item>
        <item>
            <title>Is atherosclerosis an allergic disease?</title>
            <link>http://www.medworm.com/index.php?rid=5382151&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22034478%26dopt%3DAbstract</link>
            <description>Authors: Binder CJ, Witztum JL
    PMID: 22034478 [PubMed - in process] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5382151</comments>
            <pubDate>Fri, 28 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5382151</guid>        </item>
        <item>
            <title>The Development of β-Adrenergic Receptor Antagonists for the Treatment of Heart Failure: A Paradigm for Translational Science.</title>
            <link>http://www.medworm.com/index.php?rid=5382150&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22034479%26dopt%3DAbstract</link>
            <description>Authors: Feldman AM
    PMID: 22034479 [PubMed - in process] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5382150</comments>
            <pubDate>Fri, 28 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5382150</guid>        </item>
        <item>
            <title>Treatment of Chronic Heart Failure With β-Adrenergic Receptor Antagonists: A Convergence of Receptor Pharmacology and Clinical Cardiology.</title>
            <link>http://www.medworm.com/index.php?rid=5382149&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22034480%26dopt%3DAbstract</link>
            <description>Authors: Bristow MR
    Abstract
    Despite the absence of a systematic development plan, β-blockers have reached the top tier of medical therapies for chronic heart failure. The successful outcome was due to the many dedicated investigators who produced, over a 30-year period, increasing evidence that β-blocking agents should or actually did improve the natural history of dilated cardiomyopathies and heart failure. It took 20 years for supportive evidence to become undeniable, at which time in 1993 the formidable drug development resources of large pharmaceutical companies were deployed into Phase 3 trials. Success then came relatively quickly, and within 8 years multiple agents were on the market in the United States and Europe. Importantly, there is ample room to improve antiadrenerg...</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5382149</comments>
            <pubDate>Fri, 28 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5382149</guid>        </item>
        <item>
            <title>Chromogranin B in calpain-mediated hypertrophic signaling--the chicken, the egg, or even both...?</title>
            <link>http://www.medworm.com/index.php?rid=5382148&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22034481%26dopt%3DAbstract</link>
            <description>Authors: Heidrich FM, Zhang K, Strasser RH
    PMID: 22034481 [PubMed - in process] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5382148</comments>
            <pubDate>Fri, 28 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5382148</guid>        </item>
        <item>
            <title>Thrombospondin-4 Is Required for Stretch-Mediated Contractility Augmentation in Cardiac Muscle.</title>
            <link>http://www.medworm.com/index.php?rid=5382147&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22034490%26dopt%3DAbstract</link>
            <description>Conclusion:These results identify TSP4 as myocyte-interstitial mechano-signaling molecule central to adaptive cardiac contractile responses to acute stress, which appears to play a crucial role in the transition to chronic cardiac dilatation and failure.
    PMID: 22034490 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5382147</comments>
            <pubDate>Thu, 27 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5382147</guid>        </item>
        <item>
            <title>Wnt Signaling Exerts an Antiproliferative Effect on Adult Cardiac Progenitor Cells Through IGFBP3.</title>
            <link>http://www.medworm.com/index.php?rid=5382146&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22034491%26dopt%3DAbstract</link>
            <description>Conclusions:Our study identifies canonical Wnt signaling and the novel downstream mediator, IGFBP3, as key regulators of adult cardiac progenitor self-renewal in physiological and pathological states.
    PMID: 22034491 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5382146</comments>
            <pubDate>Thu, 27 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5382146</guid>        </item>
        <item>
            <title>Analysis of Transcriptome Complexity Through RNA Sequencing in Normal and Failing Murine Hearts.</title>
            <link>http://www.medworm.com/index.php?rid=5382145&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22034492%26dopt%3DAbstract</link>
            <description>Conclusions:Our work provided a comprehensive set of methods to analyze mouse cardiac transcriptome complexity at individual exon and transcript levels. Applications of the methods may infer important new insights to gene regulation in normal and disease hearts in terms of exon utilization and potential involvement of novel components of cardiac transcriptome.
    PMID: 22034492 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5382145</comments>
            <pubDate>Thu, 27 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5382145</guid>        </item>
        <item>
            <title>B-Cell Aortic Homing and Atheroprotection Depend on Id3.</title>
            <link>http://www.medworm.com/index.php?rid=5382144&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22034493%26dopt%3DAbstract</link>
            <description>Conclusions:Together, these results are the first to identify the Id3-CCR6 pathway in B cells and demonstrate its role in aortic B-cell homing and B-cell-mediated protection from early atherosclerosis.
    PMID: 22034493 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5382144</comments>
            <pubDate>Thu, 27 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5382144</guid>        </item>
        <item>
            <title>Nitrite-Mediated S-Nitrosylation of Caspase-3 Prevents Hypoxia-Induced Endothelial Barrier Dysfunction.</title>
            <link>http://www.medworm.com/index.php?rid=5382156&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22021929%26dopt%3DAbstract</link>
            <description>Conclusions:These results are the first to demonstrate that nitrite plays a critical role in the protection of endothelial barrier function against hypoxic insult. Our findings show that nitrite holds great potential for the treatment of diseases associated with hypoxia-associated disorder of vascular homeostasis.
    PMID: 22021929 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5382156</comments>
            <pubDate>Thu, 20 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5382156</guid>        </item>
        <item>
            <title>Plasmacytoid Dendritic Cells Protect Against Atherosclerosis by Tuning T-Cell Proliferation and Activity.</title>
            <link>http://www.medworm.com/index.php?rid=5382155&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22021930%26dopt%3DAbstract</link>
            <description>Conclusions:Our data reveal a protective role for PDC in atherosclerosis, possibly by dampening T-cell proliferation and activity in peripheral lymphoid tissue, rendering PDC an interesting target for future therapeutic interventions.
    PMID: 22021930 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5382155</comments>
            <pubDate>Thu, 20 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5382155</guid>        </item>
        <item>
            <title>Nuclear Plakoglobin Is Essential for Differentiation of Cardiac Progenitor Cells to Adipocytes in Arrhythmogenic Right Ventricular Cardiomyopathy.</title>
            <link>http://www.medworm.com/index.php?rid=5382154&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22021931%26dopt%3DAbstract</link>
            <description>Conclusions:Nuclear PG provokes adipogenesis in c-Kit(+) CPCs by repressing the canonical Wnt signaling and inducing a proadipogenic gene expression. The findings suggest that adipocytes in ARVC, at least in part, originate from c-Kit(+) CPCs.
    PMID: 22021931 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5382154</comments>
            <pubDate>Thu, 20 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5382154</guid>        </item>
        <item>
            <title>Aptamer therapy for heart failure?</title>
            <link>http://www.medworm.com/index.php?rid=5331349&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21998296%26dopt%3DAbstract</link>
            <description>Authors: Port JD, Bristow MR
    PMID: 21998296 [PubMed - in process] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5331349</comments>
            <pubDate>Fri, 14 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5331349</guid>        </item>
        <item>
            <title>Irx3: a conductor of conduction.</title>
            <link>http://www.medworm.com/index.php?rid=5331348&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21998297%26dopt%3DAbstract</link>
            <description>Authors: Kelly RG
    PMID: 21998297 [PubMed - in process] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5331348</comments>
            <pubDate>Fri, 14 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5331348</guid>        </item>
        <item>
            <title>Epigenetic modifications of stem cells: a paradigm for the control of cardiac progenitor cells.</title>
            <link>http://www.medworm.com/index.php?rid=5331347&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21998298%26dopt%3DAbstract</link>
            <description>Authors: Zhou Y, Kim J, Yuan X, Braun T
    Abstract
    Stem cells of all types are characterized by the ability to self-renew and to differentiate. Multiple lines of evidence suggest that both maintenance of stemness and lineage commitment, including determination of the cardiomyogenic lineage, are tightly controlled by epigenetic mechanisms such as DNA methylation, histone modifications, and ATP-dependent chromatin remodeling. Epigenetic mechanisms are intrinsically reversible, interdependent, and highly dynamic in regulation of chromatin structure and specific gene transcription programs, thereby contributing to stem cell homeostasis. Here, we review the current understanding of epigenetic mechanisms involved in regulation of stem cell self-renewal and differentiation and in the contro...</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5331347</comments>
            <pubDate>Fri, 14 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5331347</guid>        </item>
        <item>
            <title>Caenorhabditis elegans Muscle: A Genetic and Molecular Model for Protein Interactions in the Heart.</title>
            <link>http://www.medworm.com/index.php?rid=5331346&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21998299%26dopt%3DAbstract</link>
            <description>Authors: Benian GM, Epstein HF
    Abstract
    The nematode Caenorhabditis elegans has become established as a major experimental organism with applications to many biomedical research areas. The body wall muscle cells are a useful model for the study of human cardiomyocytes and their homologous structures and proteins. The ability to readily identify mutations affecting these proteins and structures in C elegans and to be able to rigorously characterize their genotypes and phenotypes at the cellular and molecular levels permits mechanistic studies of the responsible interactions relevant to the inherited human cardiomyopathies. Future work in C elegans muscle holds great promise in uncovering new mechanisms in the pathogenesis of these cardiac disorders.
    PMID: 21998299 [PubMed - in p...</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5331346</comments>
            <pubDate>Fri, 14 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5331346</guid>        </item>
        <item>
            <title>A Novel Preclinical Strategy for Identifying Cardiotoxic Kinase Inhibitors and Mechanisms of Cardiotoxicity.</title>
            <link>http://www.medworm.com/index.php?rid=5331345&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21998323%26dopt%3DAbstract</link>
            <description>Conclusions:Zebrafish may be a valuable preclinical tool to predict cardiotoxicity. The α-adrenergic signaling pathway is an important modulator of sorafenib cardiotoxicity in vitro and in vivo and appears to act through a here-to-fore unrecognized signaling pathway downstream of α-adrenergic activation that bypasses Raf to activate ERKs.
    PMID: 21998323 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5331345</comments>
            <pubDate>Fri, 14 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5331345</guid>        </item>
        <item>
            <title>Splice Variant Specific Modulation of CaV1.2 Calcium Channel by Galectin-1 Regulates Arterial Constriction.</title>
            <link>http://www.medworm.com/index.php?rid=5331344&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21998324%26dopt%3DAbstract</link>
            <description>Conclusion:The above data indicated that Gal-1 regulates I(Ca,L) via decreasing the functional surface expression of Ca(V)1.2 channels in a splice variant selective manner and such a mechanism may play a role in modulating vascular constriction.
    PMID: 21998324 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5331344</comments>
            <pubDate>Thu, 13 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5331344</guid>        </item>
        <item>
            <title>Location Matters: Clarifying the Concept of Nuclear and Cytosolic CaMKII Subtypes.</title>
            <link>http://www.medworm.com/index.php?rid=5331343&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21998325%26dopt%3DAbstract</link>
            <description>Conclusions:These studies demonstrate that CaMKIIδ(B) and δ(C) are not exclusively restricted to the nucleus and cytosol and that spatial and functional specificity in CaMKIIδ activation is elicited by mobilization of different Ca(2+) stores rather than by compartmentalized subtype localization.
    PMID: 21998325 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5331343</comments>
            <pubDate>Thu, 13 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5331343</guid>        </item>
        <item>
            <title>Binding of CD40L to Mac-1's I-Domain Involves the EQLKKSKTL Motif and Mediates Leukocyte Recruitment and Atherosclerosis--But Does Not Affect Immunity and Thrombosis in Mice.</title>
            <link>http://www.medworm.com/index.php?rid=5331342&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21998326%26dopt%3DAbstract</link>
            <description>Conclusions:We present the novel finding that CD40L binds to the EQLKKSKTL motif on Mac-1 mediating leukocyte recruitment and atherogenesis. Specific inhibition of CD40L-Mac-1 binding may represent an attractive anti-inflammatory treatment strategy for atherosclerosis and other inflammatory conditions, potentially avoiding the unwanted immunologic and thrombotic effects of global inhibition of CD40L.
    PMID: 21998326 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5331342</comments>
            <pubDate>Thu, 13 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5331342</guid>        </item>
        <item>
            <title>Inhibition of PKC{alpha}/{beta} With Ruboxistaurin Antagonizes Heart Failure in Pigs After Myocardial Infarction Injury.</title>
            <link>http://www.medworm.com/index.php?rid=5331341&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21998327%26dopt%3DAbstract</link>
            <description>Conclusions:These results provide additional evidence in a large animal model of disease that PKCα/β inhibition (with ruboxistaurin) represents a tenable and novel therapeutic approach for treating human heart failure.
    PMID: 21998327 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5331341</comments>
            <pubDate>Thu, 13 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5331341</guid>        </item>
        <item>
            <title>CD4+ T Cells and Complement Independently Mediate Graft Ischemia in the Rejection of Mouse Orthotopic Tracheal Transplants.</title>
            <link>http://www.medworm.com/index.php?rid=5331340&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21998328%26dopt%3DAbstract</link>
            <description>Conclusions:These studies demonstrated that CD4(+) T cells and complement operate independently to cause transplant ischemia during acute rejection and that sustained ischemia is a precursor to chronic rejection.
    PMID: 21998328 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5331340</comments>
            <pubDate>Thu, 13 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5331340</guid>        </item>
        <item>
            <title>Role of KATP Channels in the Maintenance of Ventricular Fibrillation in Cardiomyopathic Human Hearts.</title>
            <link>http://www.medworm.com/index.php?rid=5300293&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21980123%26dopt%3DAbstract</link>
            <description>Conclusions:K(ATP) channel subunit gene expression is heterogeneously altered in the cardiomyopathic human heart. Blockade of K(ATP) channels promotes spontaneous defibrillation in cardiomyopathic human hearts by attenuating the ischemia-dependent spatiotemporal heterogeneity of refractoriness during early VF.
    PMID: 21980123 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5300293</comments>
            <pubDate>Thu, 06 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5300293</guid>        </item>
        <item>
            <title>Mitochondrial STAT3 Activation and Cardioprotection by Ischemic Postconditioning in Pigs With Regional Myocardial Ischemia/Reperfusion.</title>
            <link>http://www.medworm.com/index.php?rid=5300292&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21980124%26dopt%3DAbstract</link>
            <description>Conclusions:Our data support a causal role for mitochondrial STAT3 activation to mediate cardioprotection through better mitochondrial function.
    PMID: 21980124 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5300292</comments>
            <pubDate>Thu, 06 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5300292</guid>        </item>
        <item>
            <title>AMPK{alpha}2 Deletion Exacerbates Neointima Formation by Upregulating Skp2 in Vascular Smooth Muscle Cells.</title>
            <link>http://www.medworm.com/index.php?rid=5300291&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21980125%26dopt%3DAbstract</link>
            <description>Conclusions:These findings indicate that deletion of AMPKα2 through p52-Skp2-mediated ubiquintination and degradation of p27(Kip1) accentuates neointimal hyperplasia in response to wire injury.
    PMID: 21980125 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5300291</comments>
            <pubDate>Thu, 06 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5300291</guid>        </item>
        <item>
            <title>Epigenetic Regulation of Endothelial Lineage Committed Genes in Pro-Angiogenic Hematopoietic and Endothelial Progenitor Cells.</title>
            <link>http://www.medworm.com/index.php?rid=5300290&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21980126%26dopt%3DAbstract</link>
            <description>Conclusions:These findings provide evidence that histone modifications epigenetically control the eNOS promoter in proangiogenic cells.
    PMID: 21980126 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5300290</comments>
            <pubDate>Thu, 06 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5300290</guid>        </item>
        <item>
            <title>Hydrogen Sulfide as Endothelium-Derived Hyperpolarizing Factor Sulfhydrates Potassium Channels.</title>
            <link>http://www.medworm.com/index.php?rid=5300289&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21980127%26dopt%3DAbstract</link>
            <description>Conclusions:H(2)S is a major EDHF that causes vascular endothelial and smooth muscle cell hyperpolarization and vasorelaxation by activating the ATP-sensitive, intermediate conductance and small conductance potassium channels through cysteine S-sulfhydration. Because EDHF activity is a principal determinant of vasorelaxation in numerous vascular beds, drugs influencing H(2)S biosynthesis offer therapeutic potential.
    PMID: 21980127 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5300289</comments>
            <pubDate>Thu, 06 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5300289</guid>        </item>
        <item>
            <title>Induced Pluripotent Stem Cell-Derived Cardiomyocytes and Long QT Syndrome: Is Personalized Medicine Ready for Prime Time?</title>
            <link>http://www.medworm.com/index.php?rid=5282578&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21960720%26dopt%3DAbstract</link>
            <description>Authors: Priori SG
    PMID: 21960720 [PubMed - in process] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5282578</comments>
            <pubDate>Fri, 30 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5282578</guid>        </item>
        <item>
            <title>MicroRNA133a: A New Variable in Vascular Smooth Muscle Cell Phenotypic Switching.</title>
            <link>http://www.medworm.com/index.php?rid=5282577&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21960721%26dopt%3DAbstract</link>
            <description>Authors: Miano JM, Small EM
    PMID: 21960721 [PubMed - in process] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5282577</comments>
            <pubDate>Fri, 30 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5282577</guid>        </item>
        <item>
            <title>New perspectives on regeneration of the heart.</title>
            <link>http://www.medworm.com/index.php?rid=5282576&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21960722%26dopt%3DAbstract</link>
            <description>Authors: Mummery CL, Passier R
    PMID: 21960722 [PubMed - in process] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5282576</comments>
            <pubDate>Fri, 30 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5282576</guid>        </item>
        <item>
            <title>Stem cells review series: an introduction.</title>
            <link>http://www.medworm.com/index.php?rid=5282575&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21960723%26dopt%3DAbstract</link>
            <description>Authors: Dimmeler S, Losordo D
    PMID: 21960723 [PubMed - in process] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5282575</comments>
            <pubDate>Fri, 30 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5282575</guid>        </item>
        <item>
            <title>Biomaterials to enhance stem cell function in the heart.</title>
            <link>http://www.medworm.com/index.php?rid=5282574&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21960724%26dopt%3DAbstract</link>
            <description>Authors: Segers VF, Lee RT
    Abstract
    Transplantation of stem cells into the heart can improve cardiac function after myocardial infarction and in chronic heart failure, but the extent of benefit and of reproducibility of this approach are insufficient. Survival of transplanted cells into myocardium is poor, and new strategies are needed to enhance stem cell differentiation and survival in vivo. In this review, we describe how biomaterials can enhance stem cell function in the heart. Biomaterials can mimic or include naturally occurring extracellular matrix and also instruct stem cell function in different ways. Biomaterials can promote angiogenesis, enhance engraftment and differentiation of stem cells, and accelerate electromechanical integration of transplanted stem cells. Biomate...</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5282574</comments>
            <pubDate>Fri, 30 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5282574</guid>        </item>
        <item>
            <title>Mesenchymal stem cells: biology, pathophysiology, translational findings, and therapeutic implications for cardiac disease.</title>
            <link>http://www.medworm.com/index.php?rid=5282573&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21960725%26dopt%3DAbstract</link>
            <description>This article reviews the current understanding of MSC biology, mechanism of action in cardiac repair, translational findings, and early clinical trial data of MSC therapy for cardiac disease.
    PMID: 21960725 [PubMed - in process] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5282573</comments>
            <pubDate>Fri, 30 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5282573</guid>        </item>
        <item>
            <title>Role of cardiac stem cells in cardiac pathophysiology: a paradigm shift in human myocardial biology.</title>
            <link>http://www.medworm.com/index.php?rid=5282572&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21960726%26dopt%3DAbstract</link>
            <description>Authors: Leri A, Kajstura J, Anversa P
    Abstract
    For nearly a century, the human heart has been viewed as a terminally differentiated postmitotic organ in which the number of cardiomyocytes is established at birth, and these cells persist throughout the lifespan of the organ and organism. However, the discovery that cardiac stem cells live in the heart and differentiate into the various cardiac cell lineages has changed profoundly our understanding of myocardial biology. Cardiac stem cells regulate myocyte turnover and condition myocardial recovery after injury. This novel information imposes a reconsideration of the mechanisms involved in myocardial aging and the progression of cardiac hypertrophy to heart failure. Similarly, the processes implicated in the adaptation of the infarc...</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5282572</comments>
            <pubDate>Fri, 30 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5282572</guid>        </item>
        <item>
            <title>Imaging: guiding the clinical translation of cardiac stem cell therapy.</title>
            <link>http://www.medworm.com/index.php?rid=5282571&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21960727%26dopt%3DAbstract</link>
            <description>Authors: Nguyen PK, Lan F, Wang Y, Wu JC
    Abstract
    Stem cells have been touted as the holy grail of medical therapy, with promises to regenerate cardiac tissue, but it appears the jury is still out on this novel therapy. Using advanced imaging technology, scientists have discovered that these cells do not survive nor engraft long-term. In addition, only marginal benefit has been observed in large-animal studies and human trials. However, all is not lost. Further application of advanced imaging technology will help scientists unravel the mysteries of stem cell therapy and address the clinical hurdles facing its routine implementation. In this review, we will discuss how advanced imaging technology will help investigators better define the optimal delivery method, improve survival and...</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5282571</comments>
            <pubDate>Fri, 30 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5282571</guid>        </item>
        <item>
            <title>Interleukin-10 Deficiency Impairs Bone Marrow-Derived Endothelial Progenitor Cell Survival and Function in Ischemic Myocardium.</title>
            <link>http://www.medworm.com/index.php?rid=5282581&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21959218%26dopt%3DAbstract</link>
            <description>Conclusions:Taken together, our studies demonstrate that MI-induced EPC mobilization was impaired in IL-10 KO mice and that IL-10 increases EPC survival and function possibly through activation of STAT3/VEGF signaling cascades, leading to attenuation of MI-induced left ventricular dysfunction and remodeling.
    PMID: 21959218 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5282581</comments>
            <pubDate>Thu, 29 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5282581</guid>        </item>
        <item>
            <title>Rip2 Deficiency Leads to Increased Atherosclerosis Despite Decreased Inflammation.</title>
            <link>http://www.medworm.com/index.php?rid=5282580&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21959219%26dopt%3DAbstract</link>
            <description>Conclusions:Our data show that lipid accumulation and inflammation are dissociated in the vessel wall in mice with Rip2(-/-) macrophages. These results for the first time identify Rip2 as a key regulator of cellular lipid metabolism and cardiovascular disease.
    PMID: 21959219 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5282580</comments>
            <pubDate>Thu, 29 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5282580</guid>        </item>
        <item>
            <title>Histone Deacetylase 3 Regulates Smooth Muscle Differentiation in Neural Crest Cells and Development of the Cardiac Outflow Tract.</title>
            <link>http://www.medworm.com/index.php?rid=5282579&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21959220%26dopt%3DAbstract</link>
            <description>Conclusions:These results indicate that Hdac3 plays a critical and specific regulatory role in the neural crest-derived smooth muscle lineage and in formation of the OFT.
    PMID: 21959220 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5282579</comments>
            <pubDate>Thu, 29 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5282579</guid>        </item>
        <item>
            <title>Coupling of Fc{gamma} Receptor I to Fc{gamma} Receptor IIB by Src Kinase Mediates C-Reactive Protein Impairment of Endothelial Function.</title>
            <link>http://www.medworm.com/index.php?rid=5263566&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21940940%26dopt%3DAbstract</link>
            <description>Conclusions:CRP antagonism of eNOS is mediated by the coupling of FcγRI to FcγRIIB by Src kinase and resulting activation of SH2 domain-containing inositol 5'-phosphatase 1 and, consistent with this mechanism, both FcγRI and FcγRIIB are required for CRP to blunt endothelial repair in vivo. Similar mechanisms underlie eNOS antagonism by immune complex. FcγRI and FcγRIIB may be novel therapeutic targets for preventing endothelial dysfunction in inflammatory or immune complex-mediated conditions.
    PMID: 21940940 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5263566</comments>
            <pubDate>Thu, 22 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5263566</guid>        </item>
        <item>
            <title>Cardiac resynchronization therapy and reverse molecular remodeling: importance of mitochondrial redox signaling.</title>
            <link>http://www.medworm.com/index.php?rid=5234238&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21921269%26dopt%3DAbstract</link>
            <description>Authors: Zweier JL, Chen CA, Talukder MA
    PMID: 21921269 [PubMed - in process] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5234238</comments>
            <pubDate>Fri, 16 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5234238</guid>        </item>
        <item>
            <title>Immunogenicity of induced pluripotent stem cells.</title>
            <link>http://www.medworm.com/index.php?rid=5234237&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21921270%26dopt%3DAbstract</link>
            <description>Authors: Okita K, Nagata N, Yamanaka S
    PMID: 21921270 [PubMed - in process] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5234237</comments>
            <pubDate>Fri, 16 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5234237</guid>        </item>
        <item>
            <title>Twenty years of gene targeting: what we don't know.</title>
            <link>http://www.medworm.com/index.php?rid=5234236&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21921271%26dopt%3DAbstract</link>
            <description>Authors: Robbins J
    PMID: 21921271 [PubMed - in process] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5234236</comments>
            <pubDate>Fri, 16 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5234236</guid>        </item>
        <item>
            <title>Drosophila, genetic screens, and cardiac function.</title>
            <link>http://www.medworm.com/index.php?rid=5234235&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21921272%26dopt%3DAbstract</link>
            <description>Authors: Wolf MJ, Rockman HA
    Abstract
    The fruit fly, Drosophila melanogaster, has been used to study genetics, development, and signaling for nearly a century, but only over the past few decades has this tremendous resource been the focus of cardiovascular research. Fly genetics offers sophisticated transgenic systems, molecularly defined genomic deficiencies, genome-wide transgenic RNAi lines, and numerous curated mutants to perform genetic screens. As a genetically tractable model, the fly facilitates gene discovery and can complement mammalian models of disease. The circulatory system in the fly comprises well-defined sets of cardiomyocytes, and methodological advances have permitted accurate characterization of cardiac morphology and function. Thus, fly genetics and genomics of...</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5234235</comments>
            <pubDate>Fri, 16 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5234235</guid>        </item>
        <item>
            <title>Cardiovascular pharmacogenomics.</title>
            <link>http://www.medworm.com/index.php?rid=5234234&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21921273%26dopt%3DAbstract</link>
            <description>Authors: Roden DM, Johnson JA, Kimmel SE, Krauss RM, Medina MW, Shuldiner A, Wilke RA
    Abstract
    Patients vary in their responses to drug therapy, and some of that variability is genetically determined. This review outlines general approaches used to identify genetic variation that influences drug response. Examples from specific therapeutic areas are presented, such as cholesterol management, arrhythmias, heart failure, hypertension, warfarin anticoagulation, and antiplatelet agents. A brief view of potential pathways to implementation is presented.
    PMID: 21921273 [PubMed - in process] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5234234</comments>
            <pubDate>Fri, 16 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5234234</guid>        </item>
        <item>
            <title>Human Atrial Action Potential and Ca2+ Model: Sinus Rhythm and Chronic Atrial Fibrillation.</title>
            <link>http://www.medworm.com/index.php?rid=5234244&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21921263%26dopt%3DAbstract</link>
            <description>Conclusions:Our study provides a novel tool and insights into ionic bases of atrioventricular AP differences, and shows how Na(+) and Ca(2+) homeostasis critically mediate abnormal repolarization in AF.
    PMID: 21921263 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5234244</comments>
            <pubDate>Thu, 15 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5234244</guid>        </item>
        <item>
            <title>Terminal Differentiation, Advanced Organotypic Maturation, and Modeling of Hypertrophic Growth in Engineered Heart Tissue.</title>
            <link>http://www.medworm.com/index.php?rid=5234243&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21921264%26dopt%3DAbstract</link>
            <description>Conclusions:This study documents the propensity of immature cardiomyocytes to terminally differentiate and mature in EHT in a remarkably organotypic manner. It moreover provides the rationale for the utility of the EHT technology as a methodological bridge between 2D cell culture and animal models.
    PMID: 21921264 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5234243</comments>
            <pubDate>Thu, 15 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5234243</guid>        </item>
        <item>
            <title>Intrinsic Aerobic Capacity Sets a Divide for Aging and Longevity.</title>
            <link>http://www.medworm.com/index.php?rid=5234242&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21921265%26dopt%3DAbstract</link>
            <description>Conclusions:These data obtained from a contrasting heterogeneous model system provide strong evidence that genetic segregation for aerobic exercise capacity can be linked with longevity and useful for deeper mechanistic exploration.
    PMID: 21921265 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5234242</comments>
            <pubDate>Thu, 15 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5234242</guid>        </item>
        <item>
            <title>Abolishing Myofibroblast Arrhythmogeneicity by Pharmacological Ablation of {alpha}-Smooth Muscle Actin Containing Stress Fibers.</title>
            <link>http://www.medworm.com/index.php?rid=5234241&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21921266%26dopt%3DAbstract</link>
            <description>Conclusions:The results suggest that α-SMA containing stress fibers importantly contribute to myofibroblast arrhythmogeneicity. After ablation of this cytoskeletal component, cells lose their arrhythmic effects on cardiomyocytes, even if heterocellular electrotonic coupling is sustained. The findings identify α-SMA containing stress fibers as a potential future target of antiarrhythmic therapy in hearts undergoing structural remodeling.
    PMID: 21921266 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5234241</comments>
            <pubDate>Thu, 15 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5234241</guid>        </item>
        <item>
            <title>AMP-Activated Protein Kinase Regulates E3 Ligases in Rodent Heart.</title>
            <link>http://www.medworm.com/index.php?rid=5234240&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21921267%26dopt%3DAbstract</link>
            <description>Conclusions:AMPK regulates the transcription of Atrogin-1 and MuRF1 and enhances UPS-mediated protein degradation in heart. Specifically, AMPK regulates MuRF1 through the transcription factor MEF2. The absence of MuRF1 in the heart preserves cardiac function during fasting. The results strengthen the hypothesis that AMPK serves as a modulator of intracellular protein degradation in the heart.
    PMID: 21921267 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5234240</comments>
            <pubDate>Thu, 15 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5234240</guid>        </item>
        <item>
            <title>Hypoxia Is Present in Murine Atherosclerotic Plaques and Has Multiple Adverse Effects on Macrophage Lipid Metabolism.</title>
            <link>http://www.medworm.com/index.php?rid=5234239&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21921268%26dopt%3DAbstract</link>
            <description>Conclusion:Hypoxic regions are present in murine plaques. Hypoxic macrophages have increased sterol content due to the induction of sterol synthesis and the suppression of cholesterol efflux, effects that are in part mediated by HIF-1α.
    PMID: 21921268 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5234239</comments>
            <pubDate>Thu, 15 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5234239</guid>        </item>
        <item>
            <title>Differential Protein Kinase C Isoform Regulation and Increased Constitutive Activity of Acetylcholine-Regulated Potassium Channels in Atrial Remodeling.</title>
            <link>http://www.medworm.com/index.php?rid=5220076&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21903936%26dopt%3DAbstract</link>
            <description>Conclusions:PKC isoforms differentially modulate I(KACh), with conventional Ca(2+)-dependent isoforms inhibiting and novel isoforms enhancing activity. ATR causes a rate-dependent PKC isoform switch, with Ca(2+)/calpain-dependent downregulation of inhibitory PKCα and membrane translocation of stimulatory PKCε, enhancing I(KAChC). These findings provide novel insights into mechanisms underlying I(KAChC )dysregulation in AF.
    PMID: 21903936 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5220076</comments>
            <pubDate>Thu, 08 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5220076</guid>        </item>
        <item>
            <title>Phosphodiesterase 4D Regulates Baseline Sarcoplasmic Reticulum Ca2+ Release and Cardiac Contractility, Independently of L-Type Ca2+ Current.</title>
            <link>http://www.medworm.com/index.php?rid=5220075&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21903937%26dopt%3DAbstract</link>
            <description>Conclusions:PDE4D regulates basal cAMP levels in SR microdomains through its interactions with SERCA2a-PLN. Because whole-cell Ca(2+) transient amplitudes are reduced in failing human myocardium, these observations may have therapeutic implications for patients with heart failure.
    PMID: 21903937 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5220075</comments>
            <pubDate>Thu, 08 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5220075</guid>        </item>
        <item>
            <title>MicroRNA-29 in Aortic Dilation: Implications for Aneurysm Formation.</title>
            <link>http://www.medworm.com/index.php?rid=5220074&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21903938%26dopt%3DAbstract</link>
            <description>Conclusion:In conclusion, miR-29-mediated downregulation of ECM proteins may sensitize the aorta to the formation of aneurysms in advanced age. Inhibition of miR-29 in vivo abrogates aortic dilation in mice, suggesting that miR-29 may represent a novel molecular target to augment matrix synthesis and maintain vascular wall structural integrity.
    PMID: 21903938 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5220074</comments>
            <pubDate>Thu, 08 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5220074</guid>        </item>
        <item>
            <title>HCN3 Contributes to the Ventricular Action Potential Waveform in the Murine Heart.</title>
            <link>http://www.medworm.com/index.php?rid=5220073&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21903939%26dopt%3DAbstract</link>
            <description>Conclusions:We propose that HCN3 together with other members of the HCN channel family confer a depolarizing background current that regulates ventricular resting potential and counteracts the action of hyperpolarizing potassium currents in late repolarization. In conclusion, our data indicate that HCN3 plays an important role in shaping the cardiac action potential waveform.
    PMID: 21903939 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5220073</comments>
            <pubDate>Thu, 08 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5220073</guid>        </item>
        <item>
            <title>A new standard in the conflict of interest policy of the american heart association.</title>
            <link>http://www.medworm.com/index.php?rid=5194892&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21885832%26dopt%3DAbstract</link>
            <description>Authors: Bolli R
    PMID: 21885832 [PubMed - in process] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5194892</comments>
            <pubDate>Thu, 01 Sep 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5194892</guid>        </item>
        <item>
            <title>{beta}-MyHC and Cardiac Hypertrophy: Size Does Matter.</title>
            <link>http://www.medworm.com/index.php?rid=5194891&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21885833%26dopt%3DAbstract</link>
            <description>Authors: Pandya K, Smithies O
    PMID: 21885833 [PubMed - in process] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5194891</comments>
            <pubDate>Thu, 01 Sep 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5194891</guid>        </item>
        <item>
            <title>Micro-managing myocyte mitosis.</title>
            <link>http://www.medworm.com/index.php?rid=5194890&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21885834%26dopt%3DAbstract</link>
            <description>Authors: Li D, Epstein JA
    PMID: 21885834 [PubMed - in process] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5194890</comments>
            <pubDate>Thu, 01 Sep 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5194890</guid>        </item>
        <item>
            <title>Not too large and not too small-just the right size: a hippo-sized heart.</title>
            <link>http://www.medworm.com/index.php?rid=5194889&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21885835%26dopt%3DAbstract</link>
            <description>Authors: Morrisey EE
    PMID: 21885835 [PubMed - in process] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5194889</comments>
            <pubDate>Thu, 01 Sep 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5194889</guid>        </item>
        <item>
            <title>Estrogen signaling and cardiovascular disease.</title>
            <link>http://www.medworm.com/index.php?rid=5194888&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21885836%26dopt%3DAbstract</link>
            <description>This article reviews the different estrogen receptors and their signaling mechanisms, discusses mechanisms that regulate estrogen receptor levels and locations, and considers the cardiovascular effects of estrogen signaling.
    PMID: 21885836 [PubMed - in process] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5194888</comments>
            <pubDate>Thu, 01 Sep 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5194888</guid>        </item>
        <item>
            <title>Arterial calcification in chronic kidney disease: key roles for calcium and phosphate.</title>
            <link>http://www.medworm.com/index.php?rid=5194887&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21885837%26dopt%3DAbstract</link>
            <description>Authors: Shanahan CM, Crouthamel MH, Kapustin A, Giachelli CM
    Abstract
    Vascular calcification contributes to the high risk of cardiovascular mortality in chronic kidney disease (CKD) patients. Dysregulation of calcium (Ca) and phosphate (P) metabolism is common in CKD patients and drives vascular calcification. In this article, we review the physiological regulatory mechanisms for Ca and P homeostasis and the basis for their dysregulation in CKD. In addition, we highlight recent findings indicating that elevated Ca and P have direct effects on vascular smooth muscle cells (VSMCs) that promote vascular calcification, including stimulation of osteogenic/chondrogenic differentiation, vesicle release, apoptosis, loss of inhibitors, and extracellular matrix degradation. These studies su...</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5194887</comments>
            <pubDate>Thu, 01 Sep 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5194887</guid>        </item>
        <item>
            <title>Mechanism of antiarrhythmic effects of flecainide in catecholaminergic polymorphic ventricular tachycardia.</title>
            <link>http://www.medworm.com/index.php?rid=5194886&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21885838%26dopt%3DAbstract</link>
            <description>Authors: Watanabe H, Steele DS, Knollmann BC
    PMID: 21885838 [PubMed - in process] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5194886</comments>
            <pubDate>Thu, 01 Sep 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5194886</guid>        </item>
        <item>
            <title>Early Atheroma-Derived Agonists of Peroxisome Proliferator-Activated Receptor-{gamma} Trigger Intramedial Angiogenesis in a Smooth Muscle Cell-Dependent Manner.</title>
            <link>http://www.medworm.com/index.php?rid=5194895&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21885829%26dopt%3DAbstract</link>
            <description>Conclusions:We show that VEGF-A production is upregulated in medial SMCs of human atheromatous aortas and that peroxisome proliferator-activated receptor-γ agonists derived from early intimal lesions are likely to contribute to this phenotypic change. Our findings suggest that medial SMCs are central organizers of an angiogenic response initiated by the subendothelial accumulation of atherogenic lipids.
    PMID: 21885829 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5194895</comments>
            <pubDate>Wed, 31 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5194895</guid>        </item>
        <item>
            <title>p63RhoGEF Couples G{alpha}q/11-Mediated Signaling to Ca2+ Sensitization of Vascular Smooth Muscle Contractility.</title>
            <link>http://www.medworm.com/index.php?rid=5194894&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21885830%26dopt%3DAbstract</link>
            <description>Conclusion:We demonstrate that p63RhoGEF selectively couples Gα(q/11) but not Gα(12/13), to RhoA activation in blood vessels and cultured cells and thus mediates the physiologically important Ca(2+) sensitization of force induced with Gα(q/11)-coupled agonists. Our results suggest that signaling through p63RhoGEF provides a novel mechanism for selective regulation of blood pressure.
    PMID: 21885830 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5194894</comments>
            <pubDate>Wed, 31 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5194894</guid>        </item>
        <item>
            <title>Autologous Mesenchymal Stem Cells Mobilize cKit+ and CD133+ Bone Marrow Progenitor Cells and Improve Regional Function in Hibernating Myocardium.</title>
            <link>http://www.medworm.com/index.php?rid=5194893&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21885831%26dopt%3DAbstract</link>
            <description>Conclusions:Our results indicate that icMSCs improve function in hibernating myocardium independent of coronary flow or reduced scar volume. This arises from stimulation of myocyte proliferation with increases in cKit(+)/CD133(+) bone marrow progenitor cells and cKit(+)/CD133(-) resident stem cells, which increase myocyte number and reduce cellular hypertrophy.
    PMID: 21885831 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5194893</comments>
            <pubDate>Wed, 31 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5194893</guid>        </item>
        <item>
            <title>B1a B Lymphocytes Are Atheroprotective by Secreting Natural IgM That Increases IgM Deposits and Reduces Necrotic Cores in Atherosclerotic Lesions.</title>
            <link>http://www.medworm.com/index.php?rid=5179405&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21868694%26dopt%3DAbstract</link>
            <description>Conclusions:B1a lymphocytes are an atheroprotective B-lymphocyte population. Our data suggest that natural IgM secreted by these lymphocytes offers protection by depositing IgM in atherosclerotic lesions, which reduces the necrotic cores of lesions.
    PMID: 21868694 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5179405</comments>
            <pubDate>Wed, 24 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5179405</guid>        </item>
        <item>
            <title>Transplantation of Human Pericyte Progenitor Cells Improves the Repair of Infarcted Heart Through Activation of an Angiogenic Program Involving Micro-RNA-132.</title>
            <link>http://www.medworm.com/index.php?rid=5179404&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21868695%26dopt%3DAbstract</link>
            <description>Conclusion:SVP transplantation produces long-term improvement of cardiac function through a novel paracrine mechanism involving the secretion of miR-132 and inhibition of its target genes.
    PMID: 21868695 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5179404</comments>
            <pubDate>Wed, 24 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5179404</guid>        </item>
        <item>
            <title>Aptamer Neutralization of Beta1-Adrenoceptor Autoantibodies Isolated From Patients With Cardiomyopathies.</title>
            <link>http://www.medworm.com/index.php?rid=5179403&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21868696%26dopt%3DAbstract</link>
            <description>Conclusions:A specific aptamer that can neutralize cardiomyopathy associated human beta1-AABs in vitro has been identified and characterized, providing a framework for future in vivo testing of this treatment option in animal experiments.
    PMID: 21868696 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5179403</comments>
            <pubDate>Wed, 24 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5179403</guid>        </item>
        <item>
            <title>Regulatory T Cells Limit Vascular Endothelial Injury and Prevent Pulmonary Hypertension.</title>
            <link>http://www.medworm.com/index.php?rid=5179402&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21868697%26dopt%3DAbstract</link>
            <description>Conclusions:PAH may arise when regulatory T-cell (Treg) activity fails to control endothelial injury. These studies suggest that regulatory T cells normally function to limit vascular injury and may protect against the development of PAH.
    PMID: 21868697 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5179402</comments>
            <pubDate>Wed, 24 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5179402</guid>        </item>
        <item>
            <title>MicroRNA-133 Controls Vascular Smooth Muscle Cell Phenotypic Switch In Vitro and Vascular Remodeling In Vivo.</title>
            <link>http://www.medworm.com/index.php?rid=5157890&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21852550%26dopt%3DAbstract</link>
            <description>Conclusions: Our data show that miR-133 is a key regulator of vascular smooth muscle cell phenotypic switch in vitro and in vivo, suggesting its potential therapeutic application for vascular diseases.
    PMID: 21852550 [PubMed - as supplied by publisher] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5157890</comments>
            <pubDate>Thu, 18 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5157890</guid>        </item>
        <item>
            <title>Paracrine proliferative signaling by senescent cells in world health organization group 3 pulmonary hypertension: age corrupting youth?</title>
            <link>http://www.medworm.com/index.php?rid=5157881&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21852552%26dopt%3DAbstract</link>
            <description>Authors: Ryan JJ, Rehman J, Archer SL
    PMID: 21852552 [PubMed - in process] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5157881</comments>
            <pubDate>Thu, 18 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5157881</guid>        </item>
        <item>
            <title>Patching up the Myocardium.</title>
            <link>http://www.medworm.com/index.php?rid=5157880&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21852553%26dopt%3DAbstract</link>
            <description>Authors: Jay SM, Lee RT
    PMID: 21852553 [PubMed - in process] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5157880</comments>
            <pubDate>Thu, 18 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5157880</guid>        </item>
        <item>
            <title>Robert jennings: a labor of love in the laboratory.</title>
            <link>http://www.medworm.com/index.php?rid=5157879&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21852554%26dopt%3DAbstract</link>
            <description>Authors: Williams R
    PMID: 21852554 [PubMed - in process] (Source: Circulation Research)</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5157879</comments>
            <pubDate>Thu, 18 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5157879</guid>        </item>
        <item>
            <title>The regulation of valvular and vascular sclerosis by osteogenic morphogens.</title>
            <link>http://www.medworm.com/index.php?rid=5157878&amp;cid=s_38027_7_f&amp;fid=38027&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21852555%26dopt%3DAbstract</link>
            <description>Authors: Boström KI, Rajamannan NM, Towler DA
    Abstract
    Vascular calcification increasingly afflicts our aging, dysmetabolic population. Once considered only a passive process of dead and dying cells, vascular calcification has now emerged as a highly regulated form of biomineralization organized by collagenous and elastin extracellular matrices. During skeletal bone formation, paracrine epithelial-mesenchymal and endothelial-mesenchymal interactions control osteochondrocytic differentiation of multipotent mesenchymal progenitor cells. These paracrine osteogenic signals, mediated by potent morphogens of the bone morphogenetic protein and wingless-type MMTV integration site family member (Wnt) superfamilies, are also active in the programming of arterial osteoprogenitor cells during...</description>
            <author>Circulation Research</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5157878</comments>
            <pubDate>Thu, 18 Aug 2011 23:00:00 +0100</pubDate>
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