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 'Cardiovascular Research' source. Wed, 08 Feb 2012 09:32:32 +0100 http://www.medworm.com/index.php?rid=5597319&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F93%2F2%2F371%3Frss%3D1 Conclusion IBNS down-regulates TLR4 expression, NF-B activity, and IL-6 production after vascular injury. IBNS might suppress intimal hyperplasia caused by vascular inflammation such as atherosclerosis, and restenosis after angioplasty. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5597319 Mon, 16 Jan 2012 05:00:00 +0100 5597319 http://www.medworm.com/index.php?rid=5597318&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F93%2F2%2F360%3Frss%3D1 Conclusions We show for the first time that Stim1- and Orai1-mediated SOCE may be critical for Ang II-induced VSMC proliferation. This provides important information with respect to targeting cardiovascular diseases under the enhanced renin–Ang system. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5597318 Mon, 16 Jan 2012 05:00:00 +0100 5597318 http://www.medworm.com/index.php?rid=5597317&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F93%2F2%2F350%3Frss%3D1 Conclusion These results demonstrate that knockdown of NPR-A up-regulates the expression of NPR-C, Giα proteins, and NPR-C-linked AC signalling and suggests a cross-talk between NPR-A and NPR-C. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5597317 Mon, 16 Jan 2012 05:00:00 +0100 5597317 http://www.medworm.com/index.php?rid=5597316&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F93%2F2%2F340%3Frss%3D1 Conclusion These results suggest a key role of sAC in SI-induced mitochondrial Bax translocation and activation of the mitochondrial pathway of apoptosis in adult cardiomyocytes. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5597316 Mon, 16 Jan 2012 05:00:00 +0100 5597316 http://www.medworm.com/index.php?rid=5597315&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F93%2F2%2F330%3Frss%3D1 Conclusion The cardioprotective effects of PTH were shown to be independent of endogenous G-CSF release and therefore from stem cell mobilization. This puts more emphasis on the role of stem cell homing into ischaemic myocardium. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5597315 Mon, 16 Jan 2012 05:00:00 +0100 5597315 http://www.medworm.com/index.php?rid=5597314&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F93%2F2%2F320%3Frss%3D1 Conclusion Our data support the cardioprotective actions of IGF-1, which, by rescuing the mitochondrial metabolism and the energetic state of cells, reduces cell death and controls the potentially harmful autophagic response to nutritional challenges. IGF-1, therefore, may prove beneficial to mitigate damage induced by excessive nutrient-related stress, including ischaemic disease in multiple tissues. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5597314 Mon, 16 Jan 2012 05:00:00 +0100 5597314 http://www.medworm.com/index.php?rid=5597313&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F93%2F2%2F311%3Frss%3D1 Conclusion Our results suggest that selumetinib or other related inhibitors that have been safely administered to humans in clinical trials could potentially be used to treat LMNA cardiomyopathy. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5597313 Mon, 16 Jan 2012 05:00:00 +0100 5597313 http://www.medworm.com/index.php?rid=5597312&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F93%2F2%2F302%3Frss%3D1 Conclusions The results demonstrate that hypoxia induces epigenetic repression of the PKC gene through a NADPH oxidase-independent ROS-mediated pathway in the foetal heart, leading to heightened heart vulnerability to ischaemic injury in offspring. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5597312 Mon, 16 Jan 2012 05:00:00 +0100 5597312 http://www.medworm.com/index.php?rid=5597311&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F93%2F2%2F291%3Frss%3D1 Conclusion Pitx2 drives left/right patterning of the SV myocardium through multiple developmental steps. Overall, Pitx2 plays a crucial functional role by negatively modulating a nodal-type programme in the left SV myocardium. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5597311 Mon, 16 Jan 2012 05:00:00 +0100 5597311 http://www.medworm.com/index.php?rid=5597310&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F93%2F2%2F280%3Frss%3D1 Conclusion The anti-CP-7 antibody specifically inhibited the activation of α1A-AR both in vitro and in vivo. No competition binding was found between anti-CP-7 and [3H]-epinephrine or [3H]-prazosin. An antibody that specifically inhibits a receptor could be useful in research on G-protein-coupled receptors that lack specific antagonists. The antibody against the epitope CP-7 might have potential in a therapeutic application for treating primary hypertension. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5597310 Mon, 16 Jan 2012 05:00:00 +0100 5597310 http://www.medworm.com/index.php?rid=5597309&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F93%2F2%2F272%3Frss%3D1 Conclusion The ARVI is the dominant site for wavebreak at the onset of VF in normal myocardium. This may be due to the anatomic complexity of the region. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5597309 Mon, 16 Jan 2012 05:00:00 +0100 5597309 http://www.medworm.com/index.php?rid=5597308&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F93%2F2%2F263%3Frss%3D1 Conclusion Our study suggests that specific micro- and macrostructural features of the ventricle determine the incidence and spatiotemporal characteristics of conduction block, independent of spatial heterogeneities in ion channel expression. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5597308 Mon, 16 Jan 2012 05:00:00 +0100 5597308 http://www.medworm.com/index.php?rid=5597307&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F93%2F2%2F252%3Frss%3D1 Conclusion In the setting of pathological hypertrophy or heart failure, enhanced PI3Kα signalling results in the up-regulation of K+ channel subunits, normalization of K+ current densities and preserved ventricular function. Augmentation of PI3Kα signalling, therefore, may be a useful and unique strategy to protect against the increased risk of ventricular arrhythmias and sudden death associated with cardiomyopathy. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5597307 Mon, 16 Jan 2012 05:00:00 +0100 5597307 http://www.medworm.com/index.php?rid=5597306&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F93%2F2%2F242%3Frss%3D1 Conclusion Coupling of myocytes to myofibroblasts promotes EAD formation as a result of a mismatch in early vs. late repolarization reserve caused by the Ito-like component of the gap junction current. These cellular and ionic mechanisms may contribute to the pro-arrhythmic risk in fibrotic hearts. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5597306 Mon, 16 Jan 2012 05:00:00 +0100 5597306 http://www.medworm.com/index.php?rid=5597305&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F93%2F2%2F232%3Frss%3D1 Conclusion Our results unveil a novel inhibitory role for DLK1 in the regulation of angiogenesis, mediated by antagonism of the NOTCH pathway, and establish the basis for investigating its action in pathological settings. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5597305 Mon, 16 Jan 2012 05:00:00 +0100 5597305 http://www.medworm.com/index.php?rid=5597304&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F93%2F2%2F223%3Frss%3D1 Conclusion Endothelial regeneration after vascular injury did not involve circulating EPCs but was mediated solely by migration of ECs from the adjacent healthy endothelium. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5597304 Mon, 16 Jan 2012 05:00:00 +0100 5597304 http://www.medworm.com/index.php?rid=5597303&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F93%2F2%2F220%3Frss%3D1 Intercalated disc structures have conventionally been considered to be independent. Recent work shows that molecules initially thought of as belonging to one complex can actually affect another. Here, I focus on the cross-talk between connexin43 (Cx43, ‘the gap junction protein’) and the sodium channel complex and, conversely, on ankyrin-G (AnkG, a ‘component of the sodium channel complex’) and gap junctions. I speculate as to the possibility that one molecule affects the function of the other by regulating its trafficking into the intercalated disc. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5597303 Mon, 16 Jan 2012 05:00:00 +0100 5597303 http://www.medworm.com/index.php?rid=5597302&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F93%2F2%2F218%3Frss%3D1 (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5597302 Mon, 16 Jan 2012 05:00:00 +0100 5597302 http://www.medworm.com/index.php?rid=5597301&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F93%2F2%2F215%3Frss%3D1 (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5597301 Mon, 16 Jan 2012 05:00:00 +0100 5597301 http://www.medworm.com/index.php?rid=5597300&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F93%2F2%2F213%3Frss%3D1 (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5597300 Mon, 16 Jan 2012 05:00:00 +0100 5597300 http://www.medworm.com/index.php?rid=5597299&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F93%2F2%2F211%3Frss%3D1 (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5597299 Mon, 16 Jan 2012 05:00:00 +0100 5597299 http://www.medworm.com/index.php?rid=5597298&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F93%2F2%2FNP-c%3Frss%3D1 (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5597298 Mon, 16 Jan 2012 05:00:00 +0100 5597298 http://www.medworm.com/index.php?rid=5597297&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F93%2F2%2FNP-b%3Frss%3D1 (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5597297 Mon, 16 Jan 2012 05:00:00 +0100 5597297 http://www.medworm.com/index.php?rid=5597296&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F93%2F2%2FNP-a%3Frss%3D1 (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5597296 Mon, 16 Jan 2012 05:00:00 +0100 5597296 http://www.medworm.com/index.php?rid=5597295&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F93%2F2%2FNP%3Frss%3D1 (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5597295 Mon, 16 Jan 2012 05:00:00 +0100 5597295 http://www.medworm.com/index.php?rid=5524423&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F93%2F1%2F200%3Frss%3D1 Conclusion Overall our findings suggest that PI3K inhibition could be a novel tool to modulate calcium influx in vascular smooth muscle cells, thus relaxing resistance arteries and lowering blood pressure. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5524423 Mon, 19 Dec 2011 05:00:00 +0100 5524423 http://www.medworm.com/index.php?rid=5524422&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F93%2F1%2F190%3Frss%3D1 Conclusion Our data demonstrate that RIG-I signalling mediates atherosclerotic inflammation. Targeting RIG-I signalling should provide a way to inhibit atherosclerotic inflammation, which holds potential for the therapy of atherosclerosis. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5524422 Mon, 19 Dec 2011 05:00:00 +0100 5524422 http://www.medworm.com/index.php?rid=5524421&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F93%2F1%2F181%3Frss%3D1 Conclusion Cyclic mechanical stretch increases PUMA expression in cultured human VSMCs. The PUMA expression induced by stretch is mediated by IFN-, JNK, and IRF-1 pathways. These findings suggest that PUMA is an important mediator in VSMC apoptosis induced by stretch. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5524421 Mon, 19 Dec 2011 05:00:00 +0100 5524421 http://www.medworm.com/index.php?rid=5524420&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F93%2F1%2F170%3Frss%3D1 Conclusion Our findings suggest that the angiogenic effects of leptin involve sca-1+, flk-1+ vascular progenitor cells mobilized from the BM in response to ObR-mediated activation of NOX2, increased MMP9 expression, and sKitL release. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5524420 Mon, 19 Dec 2011 05:00:00 +0100 5524420 http://www.medworm.com/index.php?rid=5524419&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F93%2F1%2F162%3Frss%3D1 Conclusion HIF-1 activity in Tie2-lineage cells is required for the mobilization and homing of BMDACs to cutaneous burn wounds and for the vascularization of burn wound tissue. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5524419 Mon, 19 Dec 2011 05:00:00 +0100 5524419 http://www.medworm.com/index.php?rid=5524418&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F93%2F1%2F152%3Frss%3D1 Conclusions Shear stress increases trophoblast migration in the direction of flow, challenging the idea that trophoblasts migrate down spiral arteries retrograde to flow. This suggests that low shear stresses generated by trophoblast plugging of spiral arteries in the first trimester may favour arterial remodelling by preventing the migration with flow seen at higher shear stresses, allowing trophoblasts to migrate down the arteries in response to alternate stimuli such as uterine or endothelial cell-derived chemotactic factors. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5524418 Mon, 19 Dec 2011 05:00:00 +0100 5524418 http://www.medworm.com/index.php?rid=5524417&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F93%2F1%2F141%3Frss%3D1 Conclusion ANP enhances transendothelial caveolae-mediated albumin transport via its GC-A receptor. This ANP-mediated cross-talk between the heart and the microcirculation is critically involved in the regulation of intravascular volume. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5524417 Mon, 19 Dec 2011 05:00:00 +0100 5524417 http://www.medworm.com/index.php?rid=5524416&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F93%2F1%2F130%3Frss%3D1 Conclusion Our results highlight the pivotal role of caveolin-1 in VE-cadherin-mediated cell adhesion via catenins and, in turn, in barrier function regulation. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5524416 Mon, 19 Dec 2011 05:00:00 +0100 5524416 http://www.medworm.com/index.php?rid=5524415&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F93%2F1%2F120%3Frss%3D1 Conclusion In addition to epoxide hydrolase activity, phosphatase activity of sEH plays a pivotal role in the regulation of eNOS activity and NO-mediated EC functions. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5524415 Mon, 19 Dec 2011 05:00:00 +0100 5524415 http://www.medworm.com/index.php?rid=5524414&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F93%2F1%2F111%3Frss%3D1 Conclusion Our findings indicate an important and novel role for endothelial ARNO in VEGF-dependent initiation of angiogenesis by regulation of VEGFR-2 internalization in endothelial cells, resulting in the activation of the Akt pathway, vessel permeability, and ultimately endothelial proliferation. Thus, ARNO may be a new essential player in endothelial signalling and angiogenesis. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5524414 Mon, 19 Dec 2011 05:00:00 +0100 5524414 http://www.medworm.com/index.php?rid=5524413&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F93%2F1%2F100%3Frss%3D1 Conclusion In pressure overload, pharmacological inhibition of SMAD2 signalling attenuated cardiomyocyte hypertrophy and preserved cardiac function. SM16 prevented SMAD2-mediated downregulation of SERCA2 in vivo and in cardiomyocytes, suggesting improved cardiomyocyte Ca2+ handling as a possible cardioprotective mechanism. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5524413 Mon, 19 Dec 2011 05:00:00 +0100 5524413 http://www.medworm.com/index.php?rid=5524412&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F93%2F1%2F89%3Frss%3D1 Conclusions The results showed that post-MI exposure of rats to daily cycles of hyperoxygenation (oxygen cycling) improved stem cell engraftment, cardiac function, and increased NOS3 expression. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5524412 Mon, 19 Dec 2011 05:00:00 +0100 5524412 http://www.medworm.com/index.php?rid=5524411&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F93%2F1%2F79%3Frss%3D1 Conclusion This is the first study to demonstrate that scavenging mitochondrial reactive oxygen species (ROS) by mCAT not only attenuates most of the mitochondrial proteome changes in heart failure, but also induces a subset of unique alterations. These changes represent processes that are adaptive to the increased work and metabolic requirements of pressure overload, but which are normally inhibited by overproduction of mitochondrial ROS. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5524411 Mon, 19 Dec 2011 05:00:00 +0100 5524411 http://www.medworm.com/index.php?rid=5524410&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F93%2F1%2F69%3Frss%3D1 Conclusion Insulin inhibits myocardial AdipoR1 expression via PI3K/Akt and FoxO1 pathways, and FoxO1 mediates AdipoR1 transcription by binding to its promoter directly. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5524410 Mon, 19 Dec 2011 05:00:00 +0100 5524410 http://www.medworm.com/index.php?rid=5524409&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F93%2F1%2F60%3Frss%3D1 Conclusion These results demonstrate for the first time that EGFR plays an important role in the genesis of arrhythmias induced by reperfusion, which is likely mediated at least in part by enhancing tyrosine phosphorylation of cardiac Na+ and L-type Ca2+ channels. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5524409 Mon, 19 Dec 2011 05:00:00 +0100 5524409 http://www.medworm.com/index.php?rid=5524408&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F93%2F1%2F50%3Frss%3D1 Conclusion Organotypic heart slices represent a multicellular model of the human myocardium and a novel platform for studies ranging from the investigation of molecular interactions to tissue engineering. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5524408 Mon, 19 Dec 2011 05:00:00 +0100 5524408 http://www.medworm.com/index.php?rid=5524407&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F93%2F1%2F41%3Frss%3D1 Conclusion Short-term treatment with HDL or S1P induces phosphorylation of Cx43 by a PKC-dependent pathway. HDL-induced phosphorylation of Cx43 reduced the diffusion of large tracer molecules between cells, whereas impulse conduction was maintained. Moreover, 5 min treatment with HDL confers cardioprotection against ischaemia/reperfusion injury. These results link Cx43 for the first time to the short-term cardioprotective effects of HDL. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5524407 Mon, 19 Dec 2011 05:00:00 +0100 5524407 http://www.medworm.com/index.php?rid=5524406&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F93%2F1%2F33%3Frss%3D1 Conclusion These results indicate that decreased brain S1R contributes to the relationship between heart failure and depression in a mouse model of pressure overload. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5524406 Mon, 19 Dec 2011 05:00:00 +0100 5524406 http://www.medworm.com/index.php?rid=5524405&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F93%2F1%2F24%3Frss%3D1 Conclusion These results show that a high intake of saturated fat improves survival in heart failure compared with a high PUFA diet or low-fat diet, despite persistent mitochondrial defects. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5524405 Mon, 19 Dec 2011 05:00:00 +0100 5524405 http://www.medworm.com/index.php?rid=5524404&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F93%2F1%2F12%3Frss%3D1 Nav1.5, the pore forming α-subunit of the voltage-dependent cardiac Na+ channel, is an integral membrane protein involved in the initiation and conduction of action potentials. Mutations in the gene-encoding Nav1.5, SCN5A, have been associated with a variety of arrhythmic disorders, including long QT, Brugada, and sick sinus syndromes as well as progressive cardiac conduction defect and atrial standstill. Moreover, alterations in the Nav1.5 expression level and/or sodium current density have been frequently noticed in acquired cardiac disorders, such as heart failure. The molecular mechanisms underlying these alterations are poorly understood, but are considered essential for conception of arrhythmogenesis and the development of therapeutic strategies for prevention or treatment of a... Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5524404 Mon, 19 Dec 2011 05:00:00 +0100 5524404 http://www.medworm.com/index.php?rid=5524403&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F93%2F1%2F10%3Frss%3D1 (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5524403 Mon, 19 Dec 2011 05:00:00 +0100 5524403 http://www.medworm.com/index.php?rid=5524402&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F93%2F1%2F8%3Frss%3D1 (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5524402 Mon, 19 Dec 2011 05:00:00 +0100 5524402 http://www.medworm.com/index.php?rid=5524401&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F93%2F1%2F6%3Frss%3D1 (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5524401 Mon, 19 Dec 2011 05:00:00 +0100 5524401 http://www.medworm.com/index.php?rid=5524400&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F93%2F1%2F4%3Frss%3D1 (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5524400 Mon, 19 Dec 2011 05:00:00 +0100 5524400 http://www.medworm.com/index.php?rid=5524399&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F93%2F1%2F1%3Frss%3D1 (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5524399 Mon, 19 Dec 2011 05:00:00 +0100 5524399 http://www.medworm.com/index.php?rid=5524398&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F93%2F1%2FNP-e%3Frss%3D1 (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5524398 Mon, 19 Dec 2011 05:00:00 +0100 5524398 http://www.medworm.com/index.php?rid=5524397&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F93%2F1%2FNP-d%3Frss%3D1 (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5524397 Mon, 19 Dec 2011 05:00:00 +0100 5524397 http://www.medworm.com/index.php?rid=5524396&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F93%2F1%2FNP-c%3Frss%3D1 (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5524396 Mon, 19 Dec 2011 05:00:00 +0100 5524396 http://www.medworm.com/index.php?rid=5524395&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F93%2F1%2FNP-b%3Frss%3D1 (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5524395 Mon, 19 Dec 2011 05:00:00 +0100 5524395 http://www.medworm.com/index.php?rid=5524394&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F93%2F1%2FNP-a%3Frss%3D1 (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5524394 Mon, 19 Dec 2011 05:00:00 +0100 5524394 http://www.medworm.com/index.php?rid=5524393&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F93%2F1%2FNP%3Frss%3D1 (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5524393 Mon, 19 Dec 2011 05:00:00 +0100 5524393 http://www.medworm.com/index.php?rid=5386249&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F3%2F504%3Frss%3D1 Conclusion Activation of TRPV1 may be a novel therapeutic tool to attenuate atherosclerosis caused by a high-fat diet. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5386249 Wed, 09 Nov 2011 05:00:00 +0100 5386249 http://www.medworm.com/index.php?rid=5386248&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F3%2F494%3Frss%3D1 Conclusion Upregulation of aldolase B by accumulated fructose is a common mechanism for MG overproduction in VSMCs and aorta in different models of metabolic syndrome. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5386248 Wed, 09 Nov 2011 05:00:00 +0100 5386248 http://www.medworm.com/index.php?rid=5386247&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F3%2F484%3Frss%3D1 Conclusion PPAR inhibits vascular smooth muscle cell proliferation and migration by suppressing TLR4-mediated inflammation and ultimately attenuates intimal hyperplasia after carotid injury. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5386247 Wed, 09 Nov 2011 05:00:00 +0100 5386247 http://www.medworm.com/index.php?rid=5386246&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F3%2F476%3Frss%3D1 Conclusion These results indicate a novel role for oxLDL in promoting the mitogenic actions of C. pneumoniae in the vasculature. ERK1/2 is an important factor in the stress-mediated response and HSP60 up-regulation in VSMC. These data provide mechanistic evidence that C. pneumoniae may stimulate atherogenesis. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5386246 Wed, 09 Nov 2011 05:00:00 +0100 5386246 http://www.medworm.com/index.php?rid=5386245&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F3%2F466%3Frss%3D1 Conclusion Homocysteine up-regulates human p66shc expression via hypomethylation of specific CpG dinucleotides in the p66shc promoter, and this mechanism is important in homocysteine-induced endothelial cell dysfunction. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5386245 Wed, 09 Nov 2011 05:00:00 +0100 5386245 http://www.medworm.com/index.php?rid=5386244&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F3%2F456%3Frss%3D1 Conclusion Our studies suggest that monocyte-induced phosphorylation of MLC in ECs enhances TEM of monocytes through dissociation of EC adherens junctions. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5386244 Wed, 09 Nov 2011 05:00:00 +0100 5386244 http://www.medworm.com/index.php?rid=5386243&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F3%2F449%3Frss%3D1 Conclusion miR-126 can regulate the expression of SDF-1 in endothelial cells. In the context of an ischaemic event, systemic silencing of miR-126 leads to the mobilization of Sca-1+/Lin– progenitor cells into the peripheral circulation, potentially in response to elevated SDF-1 expression by endothelial cells present in the ischaemic tissue. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5386243 Wed, 09 Nov 2011 05:00:00 +0100 5386243 http://www.medworm.com/index.php?rid=5386242&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F3%2F439%3Frss%3D1 Conclusion Our results suggest that the depression of PI3 kinase-dependent Akt activation in response to hyperthermia in OLETF rats can be restored by candesartan. Substantial activation of the renin–angiotensin system, represented by increased myocardial AII content and subsequent PTEN phosphorylation, may underlie the pathogenesis which is ameliorated by candesartan. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5386242 Wed, 09 Nov 2011 05:00:00 +0100 5386242 http://www.medworm.com/index.php?rid=5386241&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F3%2F430%3Frss%3D1 Conclusion Our data identify PARP-2 as a mediator of DOX toxicity by regulating vascular SIRT1 activity and mitochondrial biogenesis. Moreover, to the best of our knowledge, this is the first report of SIRT1 as a protective factor in the vasculature upon oxidative stress. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5386241 Wed, 09 Nov 2011 05:00:00 +0100 5386241 http://www.medworm.com/index.php?rid=5386240&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F3%2F420%3Frss%3D1 Conclusions Our studies suggest that substance P may be important in mediating adverse myocardial remodelling secondary to volume overload by activating cardiac mast cells, leading to increased TNF-α and MMP activation with subsequent degradation of the extracellular matrix. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5386240 Wed, 09 Nov 2011 05:00:00 +0100 5386240 http://www.medworm.com/index.php?rid=5386239&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F3%2F409%3Frss%3D1 Conclusion FAK undergoes S910 phosphorylation via PKC and Src-dependent pathways that are important for cell spreading and sarcomere reorganization. Reduced FAK-S910 phosphorylation may contribute to sarcomere disorganization in DCM. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5386239 Wed, 09 Nov 2011 05:00:00 +0100 5386239 http://www.medworm.com/index.php?rid=5386238&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F3%2F401%3Frss%3D1 Conclusion Our findings suggest that attenuation of pro-inflammatory cytokines in the PVN in combination with the shift of the renin–angiotensin system towards the anti-hypertensive axis (ACE2/Ang-(1–7)/Mas) may be responsible for the overall beneficial effects of ACE2 overexpression in the PVN on the Ang II-induced hypertensive response. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5386238 Wed, 09 Nov 2011 05:00:00 +0100 5386238 http://www.medworm.com/index.php?rid=5386237&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F3%2F394%3Frss%3D1 Conclusion Thus, the second window of preconditioning normalized oxidative metabolism of LCFA during subsequent ischaemia despite elevated non-oxidative glycolysis and malonyl-CoA and was linked to protection of regional contractile function resulting in improved mechanical performance. Interestingly, the metabolic responses occurred transmurally while ischaemia was restricted solely to the subendocardium. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5386237 Wed, 09 Nov 2011 05:00:00 +0100 5386237 http://www.medworm.com/index.php?rid=5386236&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F3%2F385%3Frss%3D1 Conclusion FKN promotes myocardial injury and accelerates the progress of heart failure, which is associated with the activation of MAPKs. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5386236 Wed, 09 Nov 2011 05:00:00 +0100 5386236 http://www.medworm.com/index.php?rid=5386235&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F3%2F375%3Frss%3D1 Conclusion The increased pulmonary vascular remodelling in Alk1+/– mice leads to signs of PH and is associated with eNOS-dependent ROS production, which is preventable by anti-oxidant treatment. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5386235 Wed, 09 Nov 2011 05:00:00 +0100 5386235 http://www.medworm.com/index.php?rid=5386234&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F3%2F367%3Frss%3D1 Several studies indicate that impaired foetal growth, and in utero exposure to risk factors, especially maternal hypercholesterolaemia, may be relevant for the early onset of cardiovascular damage. The exact molecular mechanisms of such foetal programming are still unclear. Epigenetics may represent one of the possible scientific explanations of the impact of such intrauterine risk factors for the subsequent development of cardiovascular disease (CVD) during adulthood. Translational studies support this hypothesis; however, a direct causality in humans has not been ascertained. This hypothesis could be investigated in primates and in human post-mortem foetal arteries. Importantly, some studies also suggest the transgenerational transmission of epigenetic risk. The recently launched Interna... Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5386234 Wed, 09 Nov 2011 05:00:00 +0100 5386234 http://www.medworm.com/index.php?rid=5386233&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F3%2F365%3Frss%3D1 (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5386233 Wed, 09 Nov 2011 05:00:00 +0100 5386233 http://www.medworm.com/index.php?rid=5386232&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F3%2F363%3Frss%3D1 (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5386232 Wed, 09 Nov 2011 05:00:00 +0100 5386232 http://www.medworm.com/index.php?rid=5386231&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F3%2F361%3Frss%3D1 (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5386231 Wed, 09 Nov 2011 05:00:00 +0100 5386231 http://www.medworm.com/index.php?rid=5386230&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F3%2F359%3Frss%3D1 (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5386230 Wed, 09 Nov 2011 05:00:00 +0100 5386230 http://www.medworm.com/index.php?rid=5386229&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F3%2FNP-c%3Frss%3D1 (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5386229 Wed, 09 Nov 2011 05:00:00 +0100 5386229 http://www.medworm.com/index.php?rid=5386228&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F3%2FNP-b%3Frss%3D1 (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5386228 Wed, 09 Nov 2011 05:00:00 +0100 5386228 http://www.medworm.com/index.php?rid=5386227&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F3%2FNP-a%3Frss%3D1 (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5386227 Wed, 09 Nov 2011 05:00:00 +0100 5386227 http://www.medworm.com/index.php?rid=5386226&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F3%2FNP%3Frss%3D1 (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5386226 Wed, 09 Nov 2011 05:00:00 +0100 5386226 http://www.medworm.com/index.php?rid=5314323&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F2%2F358%3Frss%3D1 (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5314323 Fri, 14 Oct 2011 04:00:00 +0100 5314323 http://www.medworm.com/index.php?rid=5314322&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F2%2F348%3Frss%3D1 Conclusion Blocking AT1 receptors prevents the overexpression of CAPON and concomitant decrease in nNOS in the PVN, resulting in attenuation of sympathoexcitation commonly observed in CHF. Taken together, our data highlight the importance of altered expression and subsequent interaction of nNOS and CAPON within the PVN, leading to increased sympathoexcitation in CHF. Identifying this crucial nNOS/CAPON interaction regulated by AT1 receptors may provide an important potential therapeutic target in CHF. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5314322 Fri, 14 Oct 2011 04:00:00 +0100 5314322 http://www.medworm.com/index.php?rid=5314321&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F2%2F338%3Frss%3D1 Conclusion Lack of CD73 promotes atherogenesis most likely by de-inhibition of resident macrophages and T cells. Elevated Edn1 and TG levels may have contributed. This establishes CD73-derived adenosine as a direct or indirect regulator of atherogenesis. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5314321 Fri, 14 Oct 2011 04:00:00 +0100 5314321 http://www.medworm.com/index.php?rid=5314320&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F2%2F328%3Frss%3D1 Conclusions These data indicate that whereas serum pentameric C-reactive protein may not affect platelet activation, monomeric C-reactive protein, which dissociates from pentameric C-reactive protein on the surface of activated platelets, could contribute to atherothrombotic complications by promoting thrombosis. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5314320 Fri, 14 Oct 2011 04:00:00 +0100 5314320 http://www.medworm.com/index.php?rid=5314319&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F2%2F317%3Frss%3D1 Conclusion rTMD23 protein significantly reduces atherosclerosis and neointima formation through its thrombin-binding ability. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5314319 Fri, 14 Oct 2011 04:00:00 +0100 5314319 http://www.medworm.com/index.php?rid=5314318&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F2%2F307%3Frss%3D1 Conclusion TUDCA inhibits neointimal hyperplasia by reducing proliferation and inducing apoptosis of smooth muscle cells by suppression of ERK via PKCα-mediated MKP-1 induction. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5314318 Fri, 14 Oct 2011 04:00:00 +0100 5314318 http://www.medworm.com/index.php?rid=5314317&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F2%2F296%3Frss%3D1 Conclusion These data suggest that omentin-1 ameliorates arterial calcification and bone loss in vivo through the regulation of the RANK signalling pathway. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5314317 Fri, 14 Oct 2011 04:00:00 +0100 5314317 http://www.medworm.com/index.php?rid=5314316&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F2%2F287%3Frss%3D1 Conclusion These findings support the hypothesis that it is an accelerated fatigue-induced damage to or protease-related degradation of initially competent elastic fibres that render arteries in Marfan syndrome increasingly susceptible to dilatation, dissection, and rupture. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5314316 Fri, 14 Oct 2011 04:00:00 +0100 5314316 http://www.medworm.com/index.php?rid=5314315&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F2%2F276%3Frss%3D1 Conclusion The opposite effects of IMD on permeability of RCECs and HUVECs are due to differential regulation of actin cytoskeleton dynamics via RhoA and Rac1. Moreover, Rac1 activity is regulated by the RhoA/Rock pathway in RCECs but not in HUVECs. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5314315 Fri, 14 Oct 2011 04:00:00 +0100 5314315 http://www.medworm.com/index.php?rid=5314314&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F2%2F267%3Frss%3D1 Conclusion AVE3085 ameliorates endothelial dysfunction in db/db mice through increased NO bioavailability, which reduces oxidative stress in the vascular wall. Targeting eNOS and NO production may be a promising approach to combat diabetic vasculopathy. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5314314 Fri, 14 Oct 2011 04:00:00 +0100 5314314 http://www.medworm.com/index.php?rid=5314313&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F2%2F256%3Frss%3D1 Conclusion HIF-1α mutants were more effective for enhancing angiogenesis in ischaemic muscle tissue than wild-type HIF-1α, and the response could be qualitatively evaluated by UMI of αv-integrins expression. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5314313 Fri, 14 Oct 2011 04:00:00 +0100 5314313 http://www.medworm.com/index.php?rid=5314312&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F2%2F247%3Frss%3D1 Conclusion Hypoxia increased CT-1 levels in cardiac cells (in vitro and in vivo) through a direct regulation of CTF1 promoter by HIF-1α. This CT-1 activation by hypoxia may protect cells from apoptosis, thus supporting a protective role for CT-1 as a survival factor for cardiomyocytes. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5314312 Fri, 14 Oct 2011 04:00:00 +0100 5314312 http://www.medworm.com/index.php?rid=5314311&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F2%2F237%3Frss%3D1 Conclusion Increased glucose metabolism by itself does not trigger NADPH oxidase activation, although PPP is required to provide NOX2 with NADPH and to produce ROS. NOX2 activation results from glucose transport through SGLT1, suggesting that an extracellular metabolic signal transduces into an intracellular ionic signal. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5314311 Fri, 14 Oct 2011 04:00:00 +0100 5314311 http://www.medworm.com/index.php?rid=5314310&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F2%2F226%3Frss%3D1 Conclusions These results give new insights into the key role that TRPC channels, via interaction with the Cav1.2 channel, play in regulation of cardiac pacemaking, conduction, ventricular activity, and contractility during cardiogenesis. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5314310 Fri, 14 Oct 2011 04:00:00 +0100 5314310 http://www.medworm.com/index.php?rid=5314309&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F2%2F218%3Frss%3D1 Conclusion Our results highlight the contribution of Cx43 to the pathophysiology of AF and demonstrate the viability of gene therapy for prevention of atrial arrhythmias. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5314309 Fri, 14 Oct 2011 04:00:00 +0100 5314309 http://www.medworm.com/index.php?rid=5314308&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F2%2F209%3Frss%3D1 Conclusion A single injection of int6 siRNA promoted angiogenesis via up-regulation of HIF-2α-related angiogenic factors in the muscles of the affected hindlimb and reduced gait disturbance. The int6 gene may be a novel therapeutic target for the treatment of IC in patients with PAD. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5314308 Fri, 14 Oct 2011 04:00:00 +0100 5314308 http://www.medworm.com/index.php?rid=5314307&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F2%2F199%3Frss%3D1 Conclusion In small mesenteric arteries of ApoE–/– mice, NO-independent dilation is enhanced. Since both NO-dependent and -independent pathways can stimulate local and conducted dilation, the potential for reducing vascular resistance is improved in these vessels. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5314307 Fri, 14 Oct 2011 04:00:00 +0100 5314307 http://www.medworm.com/index.php?rid=5314306&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F2%2F191%3Frss%3D1 Prokineticins (PK1 and PK2) are peptide hormones that exert their biological activity via two common G-protein-coupled receptors: prokineticin receptor (PKR) 1 and 2. Their physiology was originally explored mostly in the context of angiogenic actions in the reproductive tract and gut motility. Since autocrine and paracrine loops have been established between PK2 and PKR1 in the heart, in this review we focus on the PK2/PKR1 signalling in the functions of the heart and kidney. PKR1 signalling is required for cardiomyocyte survival and angiogenesis. In the mouse model of myocardial infarction, intracardiac transient PKR1 transfection protects the structure and function of the heart. Gain- and loss-of-function studies reveal that PKR1 in mouse heart up-regulates its own ligand and PK2, which... Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5314306 Fri, 14 Oct 2011 04:00:00 +0100 5314306 http://www.medworm.com/index.php?rid=5314305&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F2%2F189%3Frss%3D1 (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5314305 Fri, 14 Oct 2011 04:00:00 +0100 5314305 http://www.medworm.com/index.php?rid=5314304&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F2%2F187%3Frss%3D1 (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5314304 Fri, 14 Oct 2011 04:00:00 +0100 5314304 http://www.medworm.com/index.php?rid=5314303&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F2%2F185%3Frss%3D1 (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5314303 Fri, 14 Oct 2011 04:00:00 +0100 5314303 http://www.medworm.com/index.php?rid=5314302&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F2%2F183%3Frss%3D1 (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5314302 Fri, 14 Oct 2011 04:00:00 +0100 5314302 http://www.medworm.com/index.php?rid=5314301&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F2%2FNP-c%3Frss%3D1 (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5314301 Fri, 14 Oct 2011 04:00:00 +0100 5314301 http://www.medworm.com/index.php?rid=5314300&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F2%2FNP-b%3Frss%3D1 (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5314300 Fri, 14 Oct 2011 04:00:00 +0100 5314300 http://www.medworm.com/index.php?rid=5314299&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F2%2FNP-a%3Frss%3D1 (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5314299 Fri, 14 Oct 2011 04:00:00 +0100 5314299 http://www.medworm.com/index.php?rid=5314298&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F2%2FNP%3Frss%3D1 (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5314298 Fri, 14 Oct 2011 04:00:00 +0100 5314298 http://www.medworm.com/index.php?rid=5225266&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F1%2F181%3Frss%3D1 (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5225266 Wed, 14 Sep 2011 04:00:00 +0100 5225266 http://www.medworm.com/index.php?rid=5225265&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F1%2F180-a%3Frss%3D1 (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5225265 Wed, 14 Sep 2011 04:00:00 +0100 5225265 http://www.medworm.com/index.php?rid=5225264&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F1%2F180%3Frss%3D1 (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5225264 Wed, 14 Sep 2011 04:00:00 +0100 5225264 http://www.medworm.com/index.php?rid=5225263&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F1%2F179%3Frss%3D1 (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5225263 Wed, 14 Sep 2011 04:00:00 +0100 5225263 http://www.medworm.com/index.php?rid=5225262&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F1%2F178%3Frss%3D1 (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5225262 Wed, 14 Sep 2011 04:00:00 +0100 5225262 http://www.medworm.com/index.php?rid=5225261&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F1%2F169%3Frss%3D1 Conclusion Our findings indicate differences in the magnitude of IKIR along the ILA and suggest that the influence of KIR on reactivity increases as vessel diameter decreases from proximal to distal regions. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5225261 Wed, 14 Sep 2011 04:00:00 +0100 5225261 http://www.medworm.com/index.php?rid=5225260&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F1%2F159%3Frss%3D1 Conclusion Selective, direct inhibition of FXa by rivaroxaban effectively prevented RV dysfunction and hypertrophy in MCT-injected rats, indicating a role for coagulation factors in experimental pulmonary hypertension. Clinical investigation of the impact of early and continued administration of a specific FXa inhibitor such as rivaroxaban on the course of PAH should be considered. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5225260 Wed, 14 Sep 2011 04:00:00 +0100 5225260 http://www.medworm.com/index.php?rid=5225259&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F1%2F149%3Frss%3D1 Conclusion LPA induced disruption and protection of VE-cadherin integrity through LPA1–Gi protein–Rac1–JNK/p38MAPK and LPA6–G12/13 protein–Src–C3G–Rap1 pathways, respectively. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5225259 Wed, 14 Sep 2011 04:00:00 +0100 5225259 http://www.medworm.com/index.php?rid=5225258&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F1%2F141%3Frss%3D1 Conclusion Our results confirm and extend previous findings reporting on the induction of autophagy by CSE in the lung. We show that protein damage caused by CSE activates autophagy, ultimately resulting in necrotic death of HUVECs. Via this mechanism, cigarette smoking may contribute to the deterioration of vascular endothelial function and the initiation of atherosclerosis. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5225258 Wed, 14 Sep 2011 04:00:00 +0100 5225258 http://www.medworm.com/index.php?rid=5225257&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F1%2F132%3Frss%3D1 Conclusion In addition to its documented role in the mobilization and recruitment of EPCs, our findings show that SCF directly enhances the neovascularization activity of EPCs. Furthermore, the present study provides further evidence that EPCs exhibit differentially greater responsiveness to hypoxia-inducible cytokines, including SCF, than mature endothelial cells, suggesting that EPCs in ischaemic tissues function differently from mature endothelial cells, although they exhibit very similar phenotypes. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5225257 Wed, 14 Sep 2011 04:00:00 +0100 5225257 http://www.medworm.com/index.php?rid=5225256&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F1%2F123%3Frss%3D1 Conclusion Interception of the Sdc4 pathway enhances infarct expansion and hypertrophic remodelling during early infarct healing in ischaemic–reperfusion injury and permanent infarction mouse models and exerts net beneficial effects on LV function. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5225256 Wed, 14 Sep 2011 04:00:00 +0100 5225256 http://www.medworm.com/index.php?rid=5225255&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F1%2F115%3Frss%3D1 Conclusion Our work contributes to the understanding of the earliest cardiovasculogenic events and may become an important prerequisite for cell therapy, tissue engineering, and pharmacological testing in the culture dish using pluripotent stem cell-derived as well as directly reprogrammed cardiovascular cell types. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5225255 Wed, 14 Sep 2011 04:00:00 +0100 5225255 http://www.medworm.com/index.php?rid=5225254&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F1%2F106%3Frss%3D1 Conclusions PAK1 and PP2A are integral components of a macromolecular complex with cardiac Cx43, and increased activation of associated PAK1 can contribute to enhanced Cx43 dephosphorylation and impaired intercellular coupling that may underlie slow conduction in HF. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5225254 Wed, 14 Sep 2011 04:00:00 +0100 5225254 http://www.medworm.com/index.php?rid=5225253&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F1%2F95%3Frss%3D1 Conclusion These results suggest that changes in AJ protein precede connexin43 GJ alterations, and ID remodelling might contribute to arrhythmogenesis during the development of HF. Angiotensin receptor blockade might be a new therapy for lethal ventricular arrhythmia by modulating both AJ and GJ remodelling. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5225253 Wed, 14 Sep 2011 04:00:00 +0100 5225253 http://www.medworm.com/index.php?rid=5225252&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F1%2F85%3Frss%3D1 Conclusion The present study demonstrates for the first time that mindin serves as a novel mediator that protects against cardiac hypertrophy and the transition to heart failure by blocking AKT/GSK3β and TGF-β1–Smad signalling. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5225252 Wed, 14 Sep 2011 04:00:00 +0100 5225252 http://www.medworm.com/index.php?rid=5225251&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F1%2F75%3Frss%3D1 Conclusions This study demonstrates a pro-apoptotic role of miR-195 in cardiomyocytes and identifies Sirt1 as a direct target of miR-195. The effect of miR-195 on apoptosis is mediated through down-regulation of Sirt1 and Bcl-2 and ROS production. Thus, miR-195 may be a new therapeutic target for lipotoxic cardiomyopathy. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5225251 Wed, 14 Sep 2011 04:00:00 +0100 5225251 http://www.medworm.com/index.php?rid=5225250&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F1%2F67%3Frss%3D1 Conclusion This study implicates increased INaL in excessive atrial APD prolongation and arrhythmic EAD occurrence in a congenital LQTS3 mouse model. Our observations provide the first direct demonstration of atrial EADs and triggered activity in a genetically defined animal model of human LQTS and have potential clinically-relevant mechanistic and therapeutic implications. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5225250 Wed, 14 Sep 2011 04:00:00 +0100 5225250 http://www.medworm.com/index.php?rid=5225249&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F1%2F57%3Frss%3D1 Conclusion PVA preferentially occurs in regions of enhanced NCX expression with relatively slower Ca2+ uptake and during perfusion of CPA which further reduces sarcoplasmic reticular Ca2+ uptake. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5225249 Wed, 14 Sep 2011 04:00:00 +0100 5225249 http://www.medworm.com/index.php?rid=5225248&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F1%2F48%3Frss%3D1 Conclusion In vivo, Ang II is primarily generated by ACE under basal conditions, but in inflammatory conditions, the release of MCP amplifies local Ang II concentrations and the associated inflammatory process. Thus, AT1 receptor antagonists may be more effective than ACE inhibitors for treating ongoing Ang II-mediated vascular inflammation. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5225248 Wed, 14 Sep 2011 04:00:00 +0100 5225248 http://www.medworm.com/index.php?rid=5225247&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F1%2F39%3Frss%3D1 Conclusions As a novel type of CM to FB communication, membrane nanotubes observed in vitro and in vivo provide structural and functional connectivity between CMs and FBs over long distances. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5225247 Wed, 14 Sep 2011 04:00:00 +0100 5225247 http://www.medworm.com/index.php?rid=5225246&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F1%2F29%3Frss%3D1 Conclusion PGC1β–/– hearts showed a lysophospholipid-induced cardiac lipotoxicity and impaired bioenergetics accompanied by an ion channel remodelling and altered Ca2+ homeostasis, converging to produce a ventricular arrhythmic phenotype particularly during adrenergic stress. This could contribute to the increased cardiac mortality associated with both metabolic and cardiac disease attributable to lysophospholipid accumulation. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5225246 Wed, 14 Sep 2011 04:00:00 +0100 5225246 http://www.medworm.com/index.php?rid=5225245&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F1%2F19%3Frss%3D1 The extracellular matrix protein tenascin C (TnC) is expressed in a variety of embryonic tissues, but its expression in adult arteries is co-incident with sites of vascular disease. TnC expression has been linked to the development and complications of intimal hyperplasia, pulmonary artery hypertension, atherosclerosis, myocardial infarction, and heart failure. This review identifies the growing collection of evidence linking TnC with cardiovascular disease development. The transient upregulation of this extracellular matrix protein at sites of vascular disease could provide a means to target TnC in the development of diagnostics and new therapies. Studies in TnC-deficient mice have implicated this protein in the development of intimal hyperplasia. Further animal and human studies are requ... Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5225245 Wed, 14 Sep 2011 04:00:00 +0100 5225245 http://www.medworm.com/index.php?rid=5225244&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F1%2F10%3Frss%3D1 As obesity and type 2 diabetes are becoming an epidemic in westernized countries, the incidence and prevalence of obesity- and diabetes-related co-morbidities are increasing. In type 2 diabetes ectopic lipid accumulation in the heart has been associated with cardiac dysfunction and apoptosis, a process termed lipotoxicity. Since cardiovascular diseases are the main cause of death in diabetic patients, diagnosis and treatment become increasingly important. Although ischaemic heart disease is a major problem in diabetes, non-ischaemic heart disease (better known as diabetic cardiomyopathy) becomes increasingly important with respect to the impairment of cardiac function and mortality in type 2 diabetes. The underlying aetiology of diabetic cardiomyopathy is incompletely understood but is beg... Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5225244 Wed, 14 Sep 2011 04:00:00 +0100 5225244 http://www.medworm.com/index.php?rid=5225243&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F1%2F7%3Frss%3D1 (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5225243 Wed, 14 Sep 2011 04:00:00 +0100 5225243 http://www.medworm.com/index.php?rid=5225242&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F1%2F5%3Frss%3D1 (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5225242 Wed, 14 Sep 2011 04:00:00 +0100 5225242 http://www.medworm.com/index.php?rid=5225241&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F1%2F3%3Frss%3D1 (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5225241 Wed, 14 Sep 2011 04:00:00 +0100 5225241 http://www.medworm.com/index.php?rid=5225240&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F1%2F1%3Frss%3D1 (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5225240 Wed, 14 Sep 2011 04:00:00 +0100 5225240 http://www.medworm.com/index.php?rid=5225239&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F1%2FNP-c%3Frss%3D1 (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5225239 Wed, 14 Sep 2011 04:00:00 +0100 5225239 http://www.medworm.com/index.php?rid=5225238&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F1%2FNP-b%3Frss%3D1 (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5225238 Wed, 14 Sep 2011 04:00:00 +0100 5225238 http://www.medworm.com/index.php?rid=5225237&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F1%2FNP-a%3Frss%3D1 (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5225237 Wed, 14 Sep 2011 04:00:00 +0100 5225237 http://www.medworm.com/index.php?rid=5225236&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F92%2F1%2FNP%3Frss%3D1 (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5225236 Wed, 14 Sep 2011 04:00:00 +0100 5225236 http://www.medworm.com/index.php?rid=5143646&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F91%2F4%2F743%3Frss%3D1 (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5143646 Mon, 15 Aug 2011 23:00:00 +0100 5143646 http://www.medworm.com/index.php?rid=5143645&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F91%2F4%2F742%3Frss%3D1 (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5143645 Mon, 15 Aug 2011 23:00:00 +0100 5143645 http://www.medworm.com/index.php?rid=5143644&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F91%2F4%2F732%3Frss%3D1 Conclusion Our data indicate beneficial effects of a combination of micronutritients on body weight gain, hypertriglyceridaemia, liver steatosis, and atherosclerosis in mice, and thus our findings suggest a novel cost-effective combinatorial micronutrient-based strategy worthy of being tested in humans. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5143644 Mon, 15 Aug 2011 23:00:00 +0100 5143644 http://www.medworm.com/index.php?rid=5143643&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F91%2F4%2F720%3Frss%3D1 Conclusion We demonstrate that aldosterone-mediated c-Src trafficking/activation and proinflammatory signalling involve lipid rafts/caveolae via PDGFR. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5143643 Mon, 15 Aug 2011 23:00:00 +0100 5143643 http://www.medworm.com/index.php?rid=5143642&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F91%2F4%2F711%3Frss%3D1 Conclusions The MDM2 antagonist nutlin-3 inhibits VSMC proliferation, migration, and NF-B activation, and also attenuates neointimal hyperplasia after vascular injury in mice, which is associated with suppression of vascular cell proliferation and an inflammatory response. Targeting MDM2 might be a potential therapeutic strategy for the treatment of vascular proliferative diseases. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5143642 Mon, 15 Aug 2011 23:00:00 +0100 5143642 http://www.medworm.com/index.php?rid=5143641&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F91%2F4%2F703%3Frss%3D1 Conclusion These data confirm a fundamental physiological role of medullary catecholaminergic C1 neurones in maintaining resting sympathetic vasomotor tone and arterial blood pressure. However, C1 neurones do not appear to mediate sympathoexcitation evoked by central actions of CO2. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5143641 Mon, 15 Aug 2011 23:00:00 +0100 5143641 http://www.medworm.com/index.php?rid=5143640&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F91%2F4%2F694%3Frss%3D1 Conclusion AC6, but not the closely related AC5, plays a principal role in vasodilator signalling and regulation of the membrane potential in VSMCs. These findings identify AC6 as a vital component in the vasodilatory apparatus central to the control of blood pressure. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5143640 Mon, 15 Aug 2011 23:00:00 +0100 5143640 http://www.medworm.com/index.php?rid=5143639&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F91%2F4%2F685%3Frss%3D1 Conclusion This study demonstrates the importance of bestrophins for synchronization of SMCs and strongly supports our hypothesis for generation of vasomotion. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5143639 Mon, 15 Aug 2011 23:00:00 +0100 5143639 http://www.medworm.com/index.php?rid=5143638&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F91%2F4%2F677%3Frss%3D1 Conclusion TRPM4 is critically involved in LPS-induced endothelial cell death. These results demonstrate that either pharmacological inhibition of TRPM4, suppression of TRPM4 expression, or inhibition of TRPM4 activity are able to protect endothelium against LPS injury. These results are useful in sepsis drug design and development of new strategies for sepsis therapy. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5143638 Mon, 15 Aug 2011 23:00:00 +0100 5143638 http://www.medworm.com/index.php?rid=5143637&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F91%2F4%2F668%3Frss%3D1 Conclusion These results indicate that NTs acutely modulate pulmonary endothelial NO production and contribute to relaxation of the pulmonary vasculature. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5143637 Mon, 15 Aug 2011 23:00:00 +0100 5143637 http://www.medworm.com/index.php?rid=5143636&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F91%2F4%2F659%3Frss%3D1 Conclusions Our results indicate that a vascular fat flap exerts beneficial effects on LV function and limits myocardial remodelling. Future studies must confirm whether these findings provide an alternative therapeutic approach for myocardial salvage after infarction. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5143636 Mon, 15 Aug 2011 23:00:00 +0100 5143636 http://www.medworm.com/index.php?rid=5143635&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F91%2F4%2F649%3Frss%3D1 Conclusion This meta-analysis showed that large animal models are valid to predict the outcome of clinical trials. Our results showed that cell therapy is safe and leads to a preserved LVEF. Future trials should focus on cell types other than BM-MNC, large infarction, and strategies to obtain sustained effects. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5143635 Mon, 15 Aug 2011 23:00:00 +0100 5143635 http://www.medworm.com/index.php?rid=5143634&cid=s_36718_7_f&fid=36718&url=http%3A%2F%2Fcardiovascres.oxfordjournals.org%2Fcgi%2Fcontent%2Fshort%2F91%2F4%2F640%3Frss%3D1 Conclusion IL-6-mediated induction of Th17 cells is critical for the onset of EAM, but not for its progression. IL-6/Th17 signalling could be a promising therapeutic target for the prevention of myocardial inflammation. (Source: Cardiovascular Research) Cardiovascular Research journals http://www.medworm.com/rss/comments.php?id=5143634 Mon, 15 Aug 2011 23:00:00 +0100 5143634