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        <title>Fibrogenesis and Tissue Repair 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 'Fibrogenesis and Tissue Repair' source.</description>
        <link><![CDATA[http://www.medworm.com/rss/search.php?qu=Fibrogenesis+and+Tissue+Repair&t=Fibrogenesis+and+Tissue+Repair&s=Search&f=source]]></link>
        <lastBuildDate>Thu, 09 Feb 2012 14:07:52 +0100</lastBuildDate>
        <item>
            <title>CCR6 is not necessary for functional effects of human CCL18 in a mouse model</title>
            <link>http://www.medworm.com/index.php?rid=5603720&amp;cid=s_38185_61_f&amp;fid=38185&amp;url=http%3A%2F%2Fwww.fibrogenesis.com%2Fcontent%2F5%2F1%2F2</link>
            <description>CCL18, a chemokine with no known receptor, has been implicated in several fibrotic pulmonary diseases associated with T-lymphocyte infiltration. It has been hypothesized that CCL18 may act through CCR6. Gene delivery of human CCL18 to the lungs of wild-type mice induced pulmonary infiltration of T-lymphocytes, less than 5% of which expressed CCR6. In the lungs of CCR6-deficient mice, CCL18-driven infiltration of T-lymphocytes was attenuated but not fully abrogated. It was concluded that CCR6 is not necessary for CCL18-induced changes in mice in vivo and that CCR6 is not the main functional receptor for CCL18 in this model. (Source: Fibrogenesis and Tissue Repair)</description>
            <author>Fibrogenesis and Tissue Repair</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5603720</comments>
            <pubDate>Wed, 18 Jan 2012 05:00:00 +0100</pubDate>
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        <item>
            <title>Genomics and proteomics in liver fibrosis and cirrhosis</title>
            <link>http://www.medworm.com/index.php?rid=5568613&amp;cid=s_38185_61_f&amp;fid=38185&amp;url=http%3A%2F%2Fwww.fibrogenesis.com%2Fcontent%2F5%2F1%2F1</link>
            <description>Genomics and proteomics have become increasingly important in biomedical science in the past decade, as they provide an opportunity for hypothesis-free experiments that can yield major insights not previously foreseen when scientific and clinical questions are based only on hypothesis-driven approaches. Use of these tools therefore opens new avenues for uncovering physiological and pathological pathways. Liver fibrosis is a complex disease provoked by a range of chronic injuries to the liver, amongst which are viral hepatitis, (non-) alcoholic steatohepatitis and autoimmune disorders. Some chronic liver patients will never develop fibrosis or cirrhosis, whereas others rapidly progress towards cirrhosis in a few years. This variety can be caused by disease-related factors (e.g. viral genoty...</description>
            <author>Fibrogenesis and Tissue Repair</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5568613</comments>
            <pubDate>Tue, 03 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5568613</guid>        </item>
        <item>
            <title>What is new in the liver sinusoids? Meeting report, 16th International Symposium on Cells of the Hepatic Sinusoid (ISCHS)</title>
            <link>http://www.medworm.com/index.php?rid=5500970&amp;cid=s_38185_61_f&amp;fid=38185&amp;url=http%3A%2F%2Fwww.fibrogenesis.com%2Fcontent%2F4%2F1%2F27</link>
            <description>The 16th International Symposium on cells of the hepatic Sinusoid (ISCHS) took place in Florence, Italy on September 22-24st, 2011. This meeting is a multidisciplinary meeting where new and important findings on the biology of liver cells are presented and discussed. (Source: Fibrogenesis and Tissue Repair)</description>
            <author>Fibrogenesis and Tissue Repair</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5500970</comments>
            <pubDate>Tue, 13 Dec 2011 05:00:00 +0100</pubDate>
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        <item>
            <title>Animal models for investigating chronic pancreatitis</title>
            <link>http://www.medworm.com/index.php?rid=5465031&amp;cid=s_38185_61_f&amp;fid=38185&amp;url=http%3A%2F%2Fwww.fibrogenesis.com%2Fcontent%2F4%2F1%2F26</link>
            <description>Chronic pancreatitis is defined as a continuous or recurrent inflammatory disease of the pancreas characterized by progressive and irreversible morphological changes. It typically causes pain and permanent impairment of pancreatic function. In chronic pancreatitis areas of focal necrosis are followed by perilobular and intralobular fibrosis of the parenchyma, by stone formation in the pancreatic duct, calcifications in the parenchyma as well as the formation of pseudocysts. Late in the course of the disease a progressive loss of endocrine and exocrine function occurs. Despite advances in understanding the pathogenesis no causal treatment for chronic pancreatitis is presently available. Thus, there is a need for well characterized animal models for further investigations which allow transla...</description>
            <author>Fibrogenesis and Tissue Repair</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5465031</comments>
            <pubDate>Thu, 01 Dec 2011 05:00:00 +0100</pubDate>
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        <item>
            <title>Elevation of the anti-fibrotic peptide N-acetyl-seryl-aspartyl-lysyl-proline: a blood pressure-independent beneficial effect of angiotensin I-converting enzyme inhibitors</title>
            <link>http://www.medworm.com/index.php?rid=5465032&amp;cid=s_38185_61_f&amp;fid=38185&amp;url=http%3A%2F%2Fwww.fibrogenesis.com%2Fcontent%2F4%2F1%2F25</link>
            <description>Blockade of the renin-angiotensin system (RAS) is well recognized as an essential therapy in hypertensive, heart, and kidney diseases. There are several classes of drugs that block the renin-angiotensin system; these drugs are known to exhibit anti-fibrotic action. An analysis of the molecular mechanisms of action for these drugs can reveal potential differences in their anti-fibrotic roles. In this review, we discuss the anti-fibrotic action of RAS blockade with an emphasis on the potential importance of ACE inhibition associated with the anti-fibrotic peptide N-acetyl-seryl-aspartyl-lysyl-proline (AcSDKP). (Source: Fibrogenesis and Tissue Repair)</description>
            <author>Fibrogenesis and Tissue Repair</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5465032</comments>
            <pubDate>Wed, 30 Nov 2011 05:00:00 +0100</pubDate>
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        <item>
            <title>A genetic polymorphism in the CAV1 gene associates with the development of bronchiolitis obliterans syndrome after lung transplantation</title>
            <link>http://www.medworm.com/index.php?rid=5374830&amp;cid=s_38185_61_f&amp;fid=38185&amp;url=http%3A%2F%2Fwww.fibrogenesis.com%2Fcontent%2F4%2F1%2F24</link>
            <description>A genetic polymorphism and a consequential increase in protein serum levels contribute to the development of bronchiolitis obliterans syndrome after lung transplantation. (Source: Fibrogenesis and Tissue Repair)</description>
            <author>Fibrogenesis and Tissue Repair</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5374830</comments>
            <pubDate>Tue, 01 Nov 2011 04:00:00 +0100</pubDate>
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        <item>
            <title>Chemokine (C-C motif) ligand 2 mediates direct and indirect fibrotic
responses in human and murine cultured fibrocytes</title>
            <link>http://www.medworm.com/index.php?rid=5330289&amp;cid=s_38185_61_f&amp;fid=38185&amp;url=http%3A%2F%2Fwww.fibrogenesis.com%2Fcontent%2F4%2F1%2F23</link>
            <description>Background:
Fibrocytes are a population of circulating bone marrow-derived cells that express surface markers for leukocytes and mesenchymal cells, and are capable of differentiating into myofibroblasts. They have been observed at sites of active fibrosis and increased circulating numbers correlate with mortality in idiopathic pulmonary fibrosis (IPF). Inhibition of CCR2 during experimental models of lung fibrosis reduces lung collagen deposition, as well as reducing lung fibrocyte accumulation. The aim of the present study was to determine whether human and mouse fibrocytes express functional CCR2.
Results:
Following optimized and identical human and murine fibrocyte isolation, both cell sources were shown to be positive for CCR2 by flow cytometry and this expression co-localized with col...</description>
            <author>Fibrogenesis and Tissue Repair</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5330289</comments>
            <pubDate>Wed, 19 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5330289</guid>        </item>
        <item>
            <title>Assessment of proteolytic degradation of the basement membrane:  A fragment of type IV collagen as a biochemical marker for liver fibrosis</title>
            <link>http://www.medworm.com/index.php?rid=5292635&amp;cid=s_38185_61_f&amp;fid=38185&amp;url=http%3A%2F%2Fwww.fibrogenesis.com%2Fcontent%2F4%2F1%2F22</link>
            <description>Conclusion:
This ELISA is the first assay developed for assessment of proteolytic degraded type IV collagen, which, by enabling quantification of basement membrane degradation, could be relevant in investigating various fibrogenic pathologies. The CO4-MMP degradation fragment was highly associated with liver fibrosis in the two animal models studied. (Source: Fibrogenesis and Tissue Repair)</description>
            <author>Fibrogenesis and Tissue Repair</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5292635</comments>
            <pubDate>Wed, 05 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5292635</guid>        </item>
        <item>
            <title>Plasma and cellular fibronectin: distinct and independent functions during tissue repair</title>
            <link>http://www.medworm.com/index.php?rid=5233160&amp;cid=s_38185_61_f&amp;fid=38185&amp;url=http%3A%2F%2Fwww.fibrogenesis.com%2Fcontent%2F4%2F1%2F21</link>
            <description>Fibronectin (FN) is a ubiquitous extracellular matrix (ECM) glycoprotein that plays vital roles during tissue repair. The plasma form of FN circulates in the blood and upon tissue injury is incorporated into fibrin clots in order to exert effects on platelet function and to mediate hemostasis. Cellular FN is then synthesized and assembled by cells as they migrate into the clot to reconstitute damaged tissue. The assembly of FN into a complex 3D matrix during physiological repair plays a key role not only as a structural scaffold, but also acts as a regulator of cell function during this stage of tissue repair. FN fibrillogenesis is a complex, step-wise process that is strictly regulated by a multitude of factors. During fibrosis, excessive ECM deposition is observed of which FN is one of t...</description>
            <author>Fibrogenesis and Tissue Repair</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5233160</comments>
            <pubDate>Fri, 16 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5233160</guid>        </item>
        <item>
            <title>Mesenchymal stem cells: from experiment to clinic</title>
            <link>http://www.medworm.com/index.php?rid=5203913&amp;cid=s_38185_61_f&amp;fid=38185&amp;url=http%3A%2F%2Fwww.fibrogenesis.com%2Fcontent%2F4%2F1%2F20</link>
            <description>There is much interest in adult mesenchymal stem cells (MSC) and their ability to differentiate into other cell types and partake in the anatomy and physiology of remote organs. It is now clear these cells may be purified from several organs in the body and not only the bone marrow. They take part in wound healing by contributing to myofibroblast and possibly fibroblast populations, and may be involved in epithelial tissue regeneration in certain organs, though this remains more controversial. We review the ability of MSC to modulate liver, kidney, heart and intestinal repair, and we update their opposing qualities of being less immunogenic and therefore tolerated in a transplant situation, yet may contribute to xenograft models of human tumour formation in other contexts. However, such ob...</description>
            <author>Fibrogenesis and Tissue Repair</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5203913</comments>
            <pubDate>Thu, 08 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5203913</guid>        </item>
        <item>
            <title>TLR9-induced interferon beta is associated with protection from
gammaherpesvirus-induced exacerbation of lung fibrosis</title>
            <link>http://www.medworm.com/index.php?rid=5094024&amp;cid=s_38185_61_f&amp;fid=38185&amp;url=http%3A%2F%2Fwww.fibrogenesis.com%2Fcontent%2F4%2F1%2F18</link>
            <description>${item.shortDescription} (Source: Fibrogenesis and Tissue Repair)</description>
            <author>Fibrogenesis and Tissue Repair</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5094024</comments>
            <pubDate>Mon, 01 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5094024</guid>        </item>
        <item>
            <title>Centrilobular emphysema combined with pulmonary fibrosis results in improved survival: a response</title>
            <link>http://www.medworm.com/index.php?rid=5061311&amp;cid=s_38185_61_f&amp;fid=38185&amp;url=http%3A%2F%2Fwww.fibrogenesis.com%2Fcontent%2F4%2F1%2F16</link>
            <description>${item.shortDescription} (Source: Fibrogenesis and Tissue Repair)</description>
            <author>Fibrogenesis and Tissue Repair</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5061311</comments>
            <pubDate>Sun, 24 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5061311</guid>        </item>
        <item>
            <title>Survival in pulmonary fibrosis combined with emphysema: likely defined by characteristics of specific patient subpopulations</title>
            <link>http://www.medworm.com/index.php?rid=5061310&amp;cid=s_38185_61_f&amp;fid=38185&amp;url=http%3A%2F%2Fwww.fibrogenesis.com%2Fcontent%2F4%2F1%2F17</link>
            <description>${item.shortDescription} (Source: Fibrogenesis and Tissue Repair)</description>
            <author>Fibrogenesis and Tissue Repair</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5061310</comments>
            <pubDate>Sun, 24 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5061310</guid>        </item>
        <item>
            <title>Altered monocyte and fibrocyte phenotype and function in scleroderma interstitial lung disease: reversal by caveolin-1 scaffolding domain peptide</title>
            <link>http://www.medworm.com/index.php?rid=4991602&amp;cid=s_38185_61_f&amp;fid=38185&amp;url=http%3A%2F%2Fwww.fibrogenesis.com%2Fcontent%2F4%2F1%2F15</link>
            <description>Interstitial lung disease (ILD) is a major cause of morbidity and mortality in scleroderma (systemic sclerosis, SSc). Fibrocytes are a monocyte-derived cell population implicated in the pathogenesis of fibrosing disorders. Given the recently recognized importance of caveolin-1 in regulating function and signaling in SSc monocytes, here we have examined the role of caveolin-1 in the migration/trafficking and phenotype of monocytes and fibrocytes in fibrotic lung disease in human patients and an animal model. These studies fill a gap in our understanding of how monocytes and fibrocytes contribute to SSc-ILD pathology. We find that CXCR4+/ColI+, CD34+/ColI+, and CD45+/ColI+ cells are present in SSc-ILD (but not control) lungs with CXCR4+ cells being most prevalent. Expression of CXCR4 and its...</description>
            <author>Fibrogenesis and Tissue Repair</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4991602</comments>
            <pubDate>Thu, 30 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4991602</guid>        </item>
        <item>
            <title>Elevated transforming growth factor beta and mitogen-activated protein kinase pathways mediate fibrotic traits of Dupuytren's disease fibroblasts</title>
            <link>http://www.medworm.com/index.php?rid=4974517&amp;cid=s_38185_61_f&amp;fid=38185&amp;url=http%3A%2F%2Fwww.fibrogenesis.com%2Fcontent%2F4%2F1%2F14</link>
            <description>Conclusions:
Both TGF-beta and ERK/MAP kinase pathways cooperated in mediating the enhanced proliferation and high spontaneous contraction of Dupuytren's fibroblasts. Our data indicate that both signaling pathways are prime targets for the development of non-surgical intervention strategies to treat Dupuytren's disease. (Source: Fibrogenesis and Tissue Repair)</description>
            <author>Fibrogenesis and Tissue Repair</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4974517</comments>
            <pubDate>Mon, 27 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4974517</guid>        </item>
        <item>
            <title>Thrombospondin-1 in hypoxia conditioned media blocks the growth of human microvascular endothelial cells and is increased in systemic sclerosis tissues</title>
            <link>http://www.medworm.com/index.php?rid=4891422&amp;cid=s_38185_61_f&amp;fid=38185&amp;url=http%3A%2F%2Fwww.fibrogenesis.com%2Fcontent%2F4%2F1%2F13</link>
            <description>Conclusions:
Despite the environment of chronic tissue hypoxia in SSc, there is a paradoxical absence of angiogenesis. This is thought in part due to aberrant expression of antiangiogenic factors including TSP-1. We demonstrated that TSP-1 is released in high concentrations by hypoxic endothelial cells. The conditioned media from these cells is able to block proliferation and induce apoptosis in microvascular endothelial cells - an effect that is reduced when TSP-1 is immunoprecipitated out. Further we showed that recombinant TSP-1 is able to block proliferation and induce apoptosis at concentrations consistent with those found in the plasma of patients with SSc, and that its effect occurs in the presence of elevated VEGF levels. Taken together these data are consistent with a model where ...</description>
            <author>Fibrogenesis and Tissue Repair</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4891422</comments>
            <pubDate>Wed, 01 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4891422</guid>        </item>
        <item>
            <title>Local apoptosis promotes collagen production by monocyte-derived cells in TGF-beta1-induced lung fibrosis</title>
            <link>http://www.medworm.com/index.php?rid=4839491&amp;cid=s_38185_61_f&amp;fid=38185&amp;url=http%3A%2F%2Fwww.fibrogenesis.com%2Fcontent%2F4%2F1%2F12</link>
            <description>Conclusions: Interventions that prevent collagen production by monocytes via modulation of caspase activation and of apoptosis may be ameliorative in monocyte-associated, TGF-beta1-driven processes such as pulmonary fibrosis. (Source: Fibrogenesis and Tissue Repair)</description>
            <author>Fibrogenesis and Tissue Repair</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4839491</comments>
            <pubDate>Mon, 16 May 2011 23:00:00 +0100</pubDate>
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        <item>
            <title>Epithelial to mesenchymal transition as a biomarker in renal fibrosis: are we ready for the bedside ?</title>
            <link>http://www.medworm.com/index.php?rid=4682669&amp;cid=s_38185_61_f&amp;fid=38185&amp;url=http%3A%2F%2Fwww.fibrogenesis.com%2Fcontent%2F4%2F1%2F11</link>
            <description>Over the past two decades, the concept of the epithelial to mesenchymal transition (EMT) has been imported from embryology and oncology to fibrosis, particularly in the kidney. This interest in EMT in the context of renal fibrosis stems from observations of epithelial cells undergoing phenotypic changes reminiscent of fibroblasts. Whether EMT is actually a source of interstitial fibroblasts has been the subject of heated debate, and this controversy has caused physicians to neglect the value of EMT as a biomarker in renal fibrosis. In this review, we describe the evolution of the techniques used to detect EMT during fibrosing renal diseases, and what information they provide in the diagnosis of various renal diseases. Highlighting the great heterogeneity of these techniques and the need to...</description>
            <author>Fibrogenesis and Tissue Repair</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4682669</comments>
            <pubDate>Tue, 05 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4682669</guid>        </item>
        <item>
            <title>Thrombospondin 1 is a key mediator of transforming growth factor beta-mediated cell contractility in systemic sclerosis via a mitogen-activated protein kinase kinase (MEK)/extracellular signal-regulated kinase (ERK)-dependent mechanism</title>
            <link>http://www.medworm.com/index.php?rid=4663135&amp;cid=s_38185_61_f&amp;fid=38185&amp;url=http%3A%2F%2Fwww.fibrogenesis.com%2Fcontent%2F4%2F1%2F9</link>
            <description>Conclusions:
TSP1 is a key mediator of matrix contraction of normal and systemic sclerosis fibroblasts, via MEK/ERK. (Source: Fibrogenesis and Tissue Repair)</description>
            <author>Fibrogenesis and Tissue Repair</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4663135</comments>
            <pubDate>Wed, 30 Mar 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4663135</guid>        </item>
        <item>
            <title>Ha-Ras stabilization mediates pro-fibrotic signals in dermal fibroblasts</title>
            <link>http://www.medworm.com/index.php?rid=4535384&amp;cid=s_38185_61_f&amp;fid=38185&amp;url=http%3A%2F%2Fwww.fibrogenesis.com%2Fcontent%2F4%2F1%2F8</link>
            <description>Conclusions:
Our study shows for the first time that constitutively elevated Ha-Ras protein levels can directly stimulate Smad2/3 signalling and collagen I accumulation independently of TGFbeta neo-synthesis and activation. This finding therefore implicates the Ha-Ras pathway with the early onset of fibrosis in SSc and implicitly identifies new therapeutic targets in SSc. (Source: Fibrogenesis and Tissue Repair)</description>
            <author>Fibrogenesis and Tissue Repair</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4535384</comments>
            <pubDate>Tue, 01 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4535384</guid>        </item>
        <item>
            <title>Impaired dermal wound healing in discoidin domain receptor 2-deficient mice associated with defective extracellular matrix remodeling</title>
            <link>http://www.medworm.com/index.php?rid=4428380&amp;cid=s_38185_61_f&amp;fid=38185&amp;url=http%3A%2F%2Fwww.fibrogenesis.com%2Fcontent%2F4%2F1%2F5</link>
            <description>Conclusions:
DDR2 contributes to skin fibroblast responses during tissue injury. Defective synthesis of collagen type I, crosslinking molecules and MMP2 predispose DDR2-/- mice to defective dermal wounding. (Source: Fibrogenesis and Tissue Repair)</description>
            <author>Fibrogenesis and Tissue Repair</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4428380</comments>
            <pubDate>Wed, 02 Feb 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4428380</guid>        </item>
        <item>
            <title>Cooperative interaction of CTGF and TGF-beta in animal models of fibrotic disease</title>
            <link>http://www.medworm.com/index.php?rid=4423521&amp;cid=s_38185_61_f&amp;fid=38185&amp;url=http%3A%2F%2Fwww.fibrogenesis.com%2Fcontent%2F4%2F1%2F4</link>
            <description>Background:
Connective tissue growth factor (CTGF) is widely thought to promote the development of fibrosis in collaboration with transforming growth factor beta (TGFb), however most of the evidence for its involvement comes from correlative and culture-based studies. Here, the importance of CTGF in tissue fibrosis was directly examined in three murine models of fibrotic disease: a novel model of multi-organ fibrosis induced by repeated intraperitoneal injections of CTGF and TGFb2, the unilateral ureteral obstruction (UUO) renal fibrosis model, and an intratracheal bleomycin instillation model of pulmonary fibrosis.
Results:
Intraperitoneal co-administration of CTGF and TGFb2 elicited a profound fibrotic response that was inhibited by the human anti-CTGF antibody FG-3019, as indicated by t...</description>
            <author>Fibrogenesis and Tissue Repair</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4423521</comments>
            <pubDate>Tue, 01 Feb 2011 00:00:00 +0100</pubDate>
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        <item>
            <title>Hyaluronidase recruits mesenchymal-like cells to the lung and ameliorates fibrosis</title>
            <link>http://www.medworm.com/index.php?rid=4342232&amp;cid=s_38185_61_f&amp;fid=38185&amp;url=http%3A%2F%2Fwww.fibrogenesis.com%2Fcontent%2F4%2F1%2F3</link>
            <description>In this report, we reveal that a single intranasal inoculation of HYAL induces an increase in mononuclear cells within the bronchoalveolar space demonstrating a mesenchymal-like phenotype, expressing stem cell antigen-1 (SCA-1), CD44 and CD73 but not CD34, CD45, CD3, CD4, CD8 or CD19. This influx of mesenchymal stem cell (MSC)-like cells was dependent on leukotriene production within the lung parenchyma. These findings prompted experiments demonstrating that HYAL treatment potently blocked bleomycin-induced lung injury and fibrosis while decreasing transforming growth factor (TGF)- production and collagen deposition. These data suggest that HYAL is a novel and promising tool to use autologous MSC-like cells in the treatment of pulmonary fibrosis. (Source: Fibrogenesis and Tissue Repair)</description>
            <author>Fibrogenesis and Tissue Repair</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4342232</comments>
            <pubDate>Thu, 13 Jan 2011 00:00:00 +0100</pubDate>
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        <item>
            <title>The role of fibrocytes in fibrotic diseases of the lungs and heart</title>
            <link>http://www.medworm.com/index.php?rid=4330204&amp;cid=s_38185_61_f&amp;fid=38185&amp;url=http%3A%2F%2Fwww.fibrogenesis.com%2Fcontent%2F4%2F1%2F2</link>
            <description>Fibrosis is the end result of a complex series of events that follow tissue injury and inflammation. Pathophysiologic fibrosis results in permanent scar formation, and can impair organ function. Fibrocytes are circulating, bone-marrow-derived progenitor cells that traffic from the bone marrow to the injured organ via the bloodstream, where they differentiate into fibroblasts and myofibroblasts, andplay a pivotal role in both physiologic and aberrant fibrosis. In this review, we focus on the contribution of fibrocytes to fibrotic diseases of the lungs and the heart, including interstitial lung diseases, asthma, pulmonary hypertension, atherosclerosis and ischemic cardiomyopathy. (Source: Fibrogenesis and Tissue Repair)</description>
            <author>Fibrogenesis and Tissue Repair</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4330204</comments>
            <pubDate>Mon, 10 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4330204</guid>        </item>
        <item>
            <title>Hyp-containing collagen analogs trigger the release and activation of collagen-sequestered proMMP 2 by competition with prodomain-derived peptide P33-42</title>
            <link>http://www.medworm.com/index.php?rid=4317785&amp;cid=s_38185_61_f&amp;fid=38185&amp;url=http%3A%2F%2Fwww.fibrogenesis.com%2Fcontent%2F4%2F1%2F1</link>
            <description>Conclusions:
These findings suggest novel strategies using collagen analogs for the resolution of liver fibrosis via fibrotic matrix-sequestered gelatinases. (Source: Fibrogenesis and Tissue Repair)</description>
            <author>Fibrogenesis and Tissue Repair</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4317785</comments>
            <pubDate>Thu, 06 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4317785</guid>        </item>
        <item>
            <title>Fibrillin assemblies: extracellular determinants of tissue formation and fibrosis</title>
            <link>http://www.medworm.com/index.php?rid=4224012&amp;cid=s_38185_61_f&amp;fid=38185&amp;url=http%3A%2F%2Fwww.fibrogenesis.com%2Fcontent%2F3%2F1%2F24</link>
            <description>The extracellular matrix plays a key role in tissue formation, homeostasis and repair; conversely, mutations in extracellular matrix components have catastrophic consequences for organ function and therefore, for the fitness and survival of the entire organism. Collagen, fibrillin and elastin polymers represent the architectural scaffolds that impart specific mechanic properties to tissues and organs. Fibrillin assemblies (microfibrils) have the additional function of distributing, concentrating and modulating local TGFbeta and BMP signals that regulate a plethora of cellular activities, including extracellular matrix formation and remodeling. Fibrillins also contain binding sites for integrin receptors, which induce adaptive responses to changes in the extracellular microenvironment by re...</description>
            <author>Fibrogenesis and Tissue Repair</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4224012</comments>
            <pubDate>Thu, 02 Dec 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4224012</guid>        </item>
        <item>
            <title>Toll-like receptor 2 agonists inhibit human fibrocyte differentiation</title>
            <link>http://www.medworm.com/index.php?rid=4199973&amp;cid=s_38185_61_f&amp;fid=38185&amp;url=http%3A%2F%2Fwww.fibrogenesis.com%2Fcontent%2F3%2F1%2F23</link>
            <description>Conclusions:
Our results indicate that TLR2 agonists indirectly inhibit fibrocyte differentiation and that, for some TLR2 agonists, this inhibition involves other cell types in the PBMC population secreting an unknown factor that inhibits fibrocyte differentiation. Together, these data suggest that the presence of some bacterial signals can inhibit fibrocyte differentiation and may thus slow wound closure. (Source: Fibrogenesis and Tissue Repair)</description>
            <author>Fibrogenesis and Tissue Repair</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4199973</comments>
            <pubDate>Wed, 24 Nov 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4199973</guid>        </item>
        <item>
            <title>First international summit on fibrosis in intestinal inflammation: mechanisms and biological therapies</title>
            <link>http://www.medworm.com/index.php?rid=4158257&amp;cid=s_38185_61_f&amp;fid=38185&amp;url=http%3A%2F%2Fwww.fibrogenesis.com%2Fcontent%2F3%2F1%2F22</link>
            <description>The first meeting dedicated to intestinal fibrosis entitled The First International Summit on Fibrosis in Intestinal Inflammation: Mechanisms and Biological Therapies was held in Cleveland, USA, on September 28-29, 2010. Intestinal fibrosis is a complication of inflammatory conditions affecting the small and large bowel and often results in serious clinical consequences. Despite its clinical importance the study of inflammation-driven intestinal fibrosis has received very limited attention. This explains why so little is known about its pathophysiology and the lack of significant therapeutic advances, in contrast with the recent success achieved in controlling gut inflammation with biological agents. The meeting covered most aspects directly relevant to intestinal fibrosis, including gut i...</description>
            <author>Fibrogenesis and Tissue Repair</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4158257</comments>
            <pubDate>Thu, 11 Nov 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4158257</guid>        </item>
        <item>
            <title>Toll like receptor 4 signaling in liver injury and hepatic fibrogenesis</title>
            <link>http://www.medworm.com/index.php?rid=4095828&amp;cid=s_38185_61_f&amp;fid=38185&amp;url=http%3A%2F%2Fwww.fibrogenesis.com%2Fcontent%2F3%2F1%2F21</link>
            <description>Toll like receptors (TLRs) are a family of transmembrane pattern recognition receptors (PRR) that play a key role in innate and adoptive immunity by recognizing structural components unique to bacteria, fungi and viruses. TLR4 is the most studied among TLRs, and its primary exogenous ligand is lipopolysaccharide (LPS), a component of gram-negative bacterial walls. In the absence of exogenous microbes, endogenous ligands including damage-associated molecular pattern molecules (DAMPs) from damaged matrix and injured cells can also activate TLR4 signaling. In humans, the single nucleotide polymorphisms (SNPs) of the TLR4 gene have an impact on its signal transduction and associated risks of specific diseases, including cirrhosis. In liver, TLR4 is expressed by all parenchymal and non-parenchy...</description>
            <author>Fibrogenesis and Tissue Repair</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4095828</comments>
            <pubDate>Wed, 20 Oct 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4095828</guid>        </item>
        <item>
            <title>Integrin alpha2-deficient mice provide insights into specific functions of collagen receptors in the kidney</title>
            <link>http://www.medworm.com/index.php?rid=3992519&amp;cid=s_38185_61_f&amp;fid=38185&amp;url=http%3A%2F%2Fwww.fibrogenesis.com%2Fcontent%2F3%2F1%2F19</link>
            <description>Conclusion:
These findings support our hypothesis that both these collagen receptors (ITGA2 and DDR1) play a similar role within the kidney. Further, cell-matrix interaction via collagen receptors seems to be crucial for maintenance of normal GBM architecture and function. Targeting collagen receptors such as ITGA2 might be a new form of treatment for progressive fibrotic diseases. (Source: Fibrogenesis and Tissue Repair)</description>
            <author>Fibrogenesis and Tissue Repair</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3992519</comments>
            <pubDate>Tue, 21 Sep 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3992519</guid>        </item>
        <item>
            <title>T regulatory cells and attenuated bleomycin-induced fibrosis in lungs of CCR7-/- mice</title>
            <link>http://www.medworm.com/index.php?rid=3932532&amp;cid=s_38185_61_f&amp;fid=38185&amp;url=http%3A%2F%2Fwww.fibrogenesis.com%2Fcontent%2F3%2F1%2F18</link>
            <description>Conclusions:
Our study demonstrates that the protective phenotype associated with BLM-treated CCR7-/- mice correlates with the presence of BALT and the anchoring of Tregs in the lungs of CCR7-/- mice. These data provide novel evidence to support the further investigation of CCR7-mediated Treg trafficking in the modulation of BLM-induced PF. (Source: Fibrogenesis and Tissue Repair)</description>
            <author>Fibrogenesis and Tissue Repair</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3932532</comments>
            <pubDate>Thu, 02 Sep 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3932532</guid>        </item>
        <item>
            <title>Mast cells and hypoxia drive tissue metaplasia and heterotopic ossification in idiopathic arthrofibrosis after total knee arthroplasty</title>
            <link>http://www.medworm.com/index.php?rid=3924189&amp;cid=s_38185_61_f&amp;fid=38185&amp;url=http%3A%2F%2Fwww.fibrogenesis.com%2Fcontent%2F3%2F1%2F17</link>
            <description>Conclusions:
Taken together, we suggest that hypoxia-associated oxidative stress initiates mast cell proliferation and FGF secretion, spurring fibroblast proliferation and tissue fibrosis. Fibroblasts within this hypoxic environment undergo metaplastic transformation to fibrocartilage, followed by heterotopic ossification, resulting in increased joint stiffness. Thus, hypoxia and associated oxidative stress are potential therapeutic targets for fibrosis and metaplastic progression of idiopathic arthrofibrosis after TKA. (Source: Fibrogenesis and Tissue Repair)</description>
            <author>Fibrogenesis and Tissue Repair</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3924189</comments>
            <pubDate>Tue, 31 Aug 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3924189</guid>        </item>
        <item>
            <title>The multifaceted role of pirfenidone and its novel targets</title>
            <link>http://www.medworm.com/index.php?rid=3919971&amp;cid=s_38185_61_f&amp;fid=38185&amp;url=http%3A%2F%2Fwww.fibrogenesis.com%2Fcontent%2F3%2F1%2F16</link>
            <description>Conclusions:
There is a growing understanding of the molecular effects of PFD on the wound healing mechanism, leading to novel approaches for the management of fibrosis in lung, liver and renal tissues. Although the optimum treatment for fibrosis remains undefined, it is possible that combined therapeutic regimens that include this wide-application molecule, pirfenidone, could offer a useful treatment for fibrotic disease. (Source: Fibrogenesis and Tissue Repair)</description>
            <author>Fibrogenesis and Tissue Repair</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3919971</comments>
            <pubDate>Tue, 31 Aug 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3919971</guid>        </item>
        <item>
            <title>Mesenchymal cell survival in airway and interstitial pulmonary fibrosis</title>
            <link>http://www.medworm.com/index.php?rid=3902391&amp;cid=s_38185_61_f&amp;fid=38185&amp;url=http%3A%2F%2Fwww.fibrogenesis.com%2Fcontent%2F3%2F1%2F15</link>
            <description>Fibrotic reactions in the airways of the lung or the pulmonary interstitium are a common pathologic outcome after exposure to a wide variety of toxic agents including metals, particles, or fibers. The survival of mesenchymal cells (fibroblasts and myofibroblasts) is a key factor in determining whether a fibroproliferative response that occurs after toxic injury to the lung will ultimately resolve or progress to a pathologic state. Several polypeptide growth factors, including members of the platelet-derived growth factor (PDGF) family and the epidermal growth factor (EGF) family, are pro-survival factors that stimulate a replicative and migratory mesenchymal cell phenotype during the early stages of lung fibrogenesis. This replicative phenotype can progress to a matrix synthetic phenotype ...</description>
            <author>Fibrogenesis and Tissue Repair</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3902391</comments>
            <pubDate>Tue, 24 Aug 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3902391</guid>        </item>
        <item>
            <title>Achievements and challenges in bioartificial kidney development</title>
            <link>http://www.medworm.com/index.php?rid=3853798&amp;cid=s_38185_61_f&amp;fid=38185&amp;url=http%3A%2F%2Fwww.fibrogenesis.com%2Fcontent%2F3%2F1%2F14</link>
            <description>Bioartificial kidneys (BAKs) combine a conventional hemofilter in series with a bioreactor unit containing renal epithelial cells. The epithelial cells derived from the renal tubule should provide transport, metabolic, endocrinologic and immunomodulatory functions. Currently primary human renal proximal tubule cells are most relevant for clinical applications. However, the use of human primary cells is associated with many obstacles, and the development of alternatives and an unlimited cell source is one of the most urgent challenges. BAKs have been applied in Phase I/II and Phase II clinical trials for the treatment of critically ill patients with acute renal failure. Significant effects on cytokine concentrations and long-term survival were observed. A subsequent Phase IIb clinical trial...</description>
            <author>Fibrogenesis and Tissue Repair</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3853798</comments>
            <pubDate>Mon, 09 Aug 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3853798</guid>        </item>
        <item>
            <title>Angiogenesis and chronic kidney disease</title>
            <link>http://www.medworm.com/index.php?rid=3826460&amp;cid=s_38185_61_f&amp;fid=38185&amp;url=http%3A%2F%2Fwww.fibrogenesis.com%2Fcontent%2F3%2F1%2F13</link>
            <description>The number of patients requiring renal replacement therapy due to end-stage renal disease (ESRD) is increasing worldwide. The prevalence of Chronic Kidney Disease (CKD) as well as the importance of CKD as a risk factor for developing ESRD and complicating cardiovascular disease (CVD) have been clarified. In recent years, the involvement of angiogenesis-related factors in the progression of CKD and potential therapeutic approaches on CKD by modulating these factors, have been studied. Vascular endothelial growth factor (VEGF)-A, a potent pro-angiogenic factor, is involved in the development of kidney, maintenance of the glomerular capillary structure and filtration barrier, and renal repair process following injuries. VEGF-A is also involved in the development of early diabetic nephropathy,...</description>
            <author>Fibrogenesis and Tissue Repair</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3826460</comments>
            <pubDate>Wed, 04 Aug 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3826460</guid>        </item>
        <item>
            <title>Interstitial fluid: the overlooked component of the tumor microenvironment?</title>
            <link>http://www.medworm.com/index.php?rid=3783681&amp;cid=s_38185_61_f&amp;fid=38185&amp;url=http%3A%2F%2Fwww.fibrogenesis.com%2Fcontent%2F3%2F1%2F12</link>
            <description>Conclusions:
Access to fluid that reliably reflects the local microenvironment enables us to identify substances that can be used in early detection and monitoring of disease. (Source: Fibrogenesis and Tissue Repair)</description>
            <author>Fibrogenesis and Tissue Repair</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3783681</comments>
            <pubDate>Thu, 22 Jul 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3783681</guid>        </item>
        <item>
            <title>Serum amyloid P ameliorates radiation-induced oral mucositis and fibrosis</title>
            <link>http://www.medworm.com/index.php?rid=3726317&amp;cid=s_38185_61_f&amp;fid=38185&amp;url=http%3A%2F%2Fwww.fibrogenesis.com%2Fcontent%2F3%2F1%2F11</link>
            <description>Conclusions:
SAP treatment significantly attenuated radiation-induced injury. In particular, SAP attenuated the severity of OM and inhibited pathogenic remodeling. This suggests that SAP may be a useful therapy for the palliation of side effects observed during treatment for head and neck cancer. (Source: Fibrogenesis and Tissue Repair)</description>
            <author>Fibrogenesis and Tissue Repair</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3726317</comments>
            <pubDate>Sun, 04 Jul 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3726317</guid>        </item>
        <item>
            <title>Development and evaluation of an open source Delphi-based 
software for morphometric quantification of liver fibrosis</title>
            <link>http://www.medworm.com/index.php?rid=3670764&amp;cid=s_38185_61_f&amp;fid=38185&amp;url=http%3A%2F%2Fwww.fibrogenesis.com%2Fcontent%2F3%2F1%2F10</link>
            <description>Conclusions:
Using our Delphi-based image analysing software, the morphometric assessment of fibrosis is as precise as semi-quantitative scoring by an experienced pathologist. This program can be a valuable tool in any kind of experimental or clinical setting for standardized quantitative assessment of fibrosis. (Source: Fibrogenesis and Tissue Repair)</description>
            <author>Fibrogenesis and Tissue Repair</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3670764</comments>
            <pubDate>Wed, 16 Jun 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3670764</guid>        </item>
        <item>
            <title>Interleukins 4 and 13 modulate gene expression and promote proliferation of primary human tenocytes</title>
            <link>http://www.medworm.com/index.php?rid=3647861&amp;cid=s_38185_61_f&amp;fid=38185&amp;url=http%3A%2F%2Fwww.fibrogenesis.com%2Fcontent%2F3%2F1%2F9</link>
            <description>Conclusions:
Stimulation with IL-4 or IL-13 could be used to facilitate tendon repair in vivo or to aid in tendon tissue engineering, through stimulation of tenocyte proliferation. (Source: Fibrogenesis and Tissue Repair)</description>
            <author>Fibrogenesis and Tissue Repair</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3647861</comments>
            <pubDate>Wed, 09 Jun 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3647861</guid>        </item>
        <item>
            <title>Towards an anti-fibrotic therapy for scleroderma: targeting myofibroblast differentiation and recruitment</title>
            <link>http://www.medworm.com/index.php?rid=3602885&amp;cid=s_38185_61_f&amp;fid=38185&amp;url=http%3A%2F%2Fwww.fibrogenesis.com%2Fcontent%2F3%2F1%2F8</link>
            <description>Conclusions:
TGFbeta, ET-1, CCN2 and PDGF are likely to cooperate in driving tissue repair and fibrogenic responses in fibroblasts. TGFbeta, ET-1 and CCN2 appear to contribute to myofibroblast differentiation; PDGF appears to be involved with pericyte recruitment. Thus, different therapeutic strategies may exist for targeting the multisystem fibrotic disorder SSc. (Source: Fibrogenesis and Tissue Repair)</description>
            <author>Fibrogenesis and Tissue Repair</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3602885</comments>
            <pubDate>Wed, 26 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3602885</guid>        </item>
        <item>
            <title>The role of renin angiotensin system inhibition in kidney repair</title>
            <link>http://www.medworm.com/index.php?rid=3529141&amp;cid=s_38185_61_f&amp;fid=38185&amp;url=http%3A%2F%2Fwww.fibrogenesis.com%2Fcontent%2F3%2F1%2F7</link>
            <description>Chronic kidney diseases share common pathogenic mechanisms that, independently from the initial injury, lead to glomerular hyperfiltration, proteinuria, and progressive renal scarring and function loss. Inhibition of the renin angiotensin system (RAS) has been consistently found to reduce or halt the progressive deterioration of renal function through reduction of blood pressure and proteinuria, the two main determinants of renal function decline. In few instances, RAS inhibition may even promote amelioration of the glomerular filtration rate. Animal data suggest that chronic therapy with angiotensin-converting enzyme inhibitors or angiotensin II receptor type I blockers promotes regression of glomerulosclerosis, even in later phases of the disease. In humans, studies investigating the eff...</description>
            <author>Fibrogenesis and Tissue Repair</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3529141</comments>
            <pubDate>Mon, 03 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3529141</guid>        </item>
        <item>
            <title>Procollagen type I N-terminal propeptide (PINP) is a marker for fibrogenesis in bile duct ligation-induced fibrosis in rats</title>
            <link>http://www.medworm.com/index.php?rid=3428337&amp;cid=s_38185_61_f&amp;fid=38185&amp;url=http%3A%2F%2Fwww.fibrogenesis.com%2Fcontent%2F3%2F1%2F5</link>
            <description>Conclusion:
PINP was associated with the development of liver fibrosis, but not bone formation, in mature rats subjected to BDL. Thus, PINP may be useful in studying the pathogenesis of liver fibrosis. However, caution should be applied when interpreting PINP levels in other disease states. (Source: Fibrogenesis and Tissue Repair)</description>
            <author>Fibrogenesis and Tissue Repair</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3428337</comments>
            <pubDate>Wed, 31 Mar 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3428337</guid>        </item>
        <item>
            <title>A novel soft-tissue in vitro model for bisphosphonate-associated osteonecrosis</title>
            <link>http://www.medworm.com/index.php?rid=3428336&amp;cid=s_38185_61_f&amp;fid=38185&amp;url=http%3A%2F%2Fwww.fibrogenesis.com%2Fcontent%2F3%2F1%2F6</link>
            <description>Conclusions:
The results from this study demonstrate that low concentrations of ZA released from bone can rapidly and directly affect the oral mucosal tissues, initially through the induction of apoptosis and long term through the inhibition of cell proliferation. These findings provide an in vitro model for a soft-tissue mechanistic component in the initiation and/or progression of ONJ. (Source: Fibrogenesis and Tissue Repair)</description>
            <author>Fibrogenesis and Tissue Repair</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3428336</comments>
            <pubDate>Wed, 31 Mar 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3428336</guid>        </item>
        <item>
            <title>Epithelial-mesenchymal transition in primary human bronchial epithelial cells is Smad-dependent and enhanced by fibronectin and TNF-alpha</title>
            <link>http://www.medworm.com/index.php?rid=3141879&amp;cid=s_38185_61_f&amp;fid=38185&amp;url=http%3A%2F%2Fwww.fibrogenesis.com%2Fcontent%2F3%2F1%2F2</link>
            <description>Conclusions:
The results presented in this study provide additional insights into EMT, a potentially very important mechanism in fibrogenesis. We show that, in addition to alveolar epithelial type II cells, primary HBECs are also able to undergo EMT in vitro upon TGF-beta1 stimulation via a primarily Smad 2/3 dependent mechanism. The effect of TGF-beta1 is potentiated on fibronectin matrix and in the presence of TNF-alpha, representing a millieu reminiscent of fibrotic lesions. Our results can contribute to a better understanding of lung fibrosis and to the development of new therapeutic approaches. (Source: Fibrogenesis and Tissue Repair)</description>
            <author>Fibrogenesis and Tissue Repair</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3141879</comments>
            <pubDate>Tue, 05 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3141879</guid>        </item>
        <item>
            <title>The Pin 1 inhibitor juglone attenuates kidney fibrogenesis via Pin 1-independent mechanisms in the unilateral ureteral occlusion model</title>
            <link>http://www.medworm.com/index.php?rid=3138712&amp;cid=s_38185_61_f&amp;fid=38185&amp;url=http%3A%2F%2Fwww.fibrogenesis.com%2Fcontent%2F3%2F1%2F1</link>
            <description>Conclusions:
Juglone attenuates fibrogenesis via Pin 1-independent mechanisms in the UUO model. The antifibrotic effects of juglone may result from the inhibition of smad2 and oxidative stress. (Source: Fibrogenesis and Tissue Repair)</description>
            <author>Fibrogenesis and Tissue Repair</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3138712</comments>
            <pubDate>Mon, 04 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3138712</guid>        </item>
        <item>
            <title>Focus on collagen: in vitro systems to study fibrogenesis and antifibrosis -- state of the art</title>
            <link>http://www.medworm.com/index.php?rid=3088665&amp;cid=s_38185_61_f&amp;fid=38185&amp;url=http%3A%2F%2Fwww.fibrogenesis.com%2Fcontent%2F2%2F1%2F7</link>
            <description>Fibrosis represents a major global disease burden, yet a potent antifibrotic compound is still not in sight. Part of the explanation for this situation is the difficulties that both academic laboratories and research and development departments in the pharmaceutical industry have been facing in re-enacting the fibrotic process in vitro for screening procedures prior to animal testing. Effective in vitro characterization of antifibrotic compounds has been hampered by cell culture settings that are lacking crucial cofactors or are not holistic representations of the biosynthetic and depositional pathway leading to the formation of an insoluble pericellular collagen matrix. In order to appreciate the task which in vitro screening of antifibrotics is up against, we will first review the fibrot...</description>
            <author>Fibrogenesis and Tissue Repair</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3088665</comments>
            <pubDate>Tue, 15 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3088665</guid>        </item>
        <item>
            <title>Reactive oxygen and nitrogen species induce protein and DNA modifications driving arthrofibrosis following total knee arthroplasty</title>
            <link>http://www.medworm.com/index.php?rid=2988345&amp;cid=s_38185_61_f&amp;fid=38185&amp;url=http%3A%2F%2Fwww.fibrogenesis.com%2Fcontent%2F2%2F1%2F5</link>
            <description>Conclusions:
Based on our current findings, we suggest that ROS/RNS initiate and sustain the arthrofibrotic response driving aggressive fibroblast proliferation and subsequent HO. (Source: Fibrogenesis and Tissue Repair)</description>
            <author>Fibrogenesis and Tissue Repair</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2988345</comments>
            <pubDate>Fri, 13 Nov 2009 00:00:00 +0100</pubDate>
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            <title>Hepatic wound repair</title>
            <link>http://www.medworm.com/index.php?rid=2831485&amp;cid=s_38185_61_f&amp;fid=38185&amp;url=http%3A%2F%2Fwww.fibrogenesis.com%2Fcontent%2F2%2F1%2F4</link>
            <description>Conclusions:
Emerging mechanisms and concepts related to liver fibrogenesis may significantly contribute to clinical management of patients affected by CLDs. (Source: Fibrogenesis and Tissue Repair)</description>
            <author>Fibrogenesis and Tissue Repair</author>
            <type>journals</type>
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            <pubDate>Thu, 24 Sep 2009 23:00:00 +0100</pubDate>
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            <title>Regression of fibrosis in paediatric autoimmune hepatitis: morphometric assessment of fibrosis versus semiquantiatative methods</title>
            <link>http://www.medworm.com/index.php?rid=2323435&amp;cid=s_38185_61_f&amp;fid=38185&amp;url=http%3A%2F%2Fwww.fibrogenesis.com%2Fcontent%2F2%2F1%2F2</link>
            <description>Conclusions:
Significant regression of fibrosis in paediatric AIH could occur with current therapeutic regimens. Morphometric assessment of fibrosis is more sensitive than semi-quantitative methods to identify changes in fibrosis. (Source: Fibrogenesis and Tissue Repair)</description>
            <author>Fibrogenesis and Tissue Repair</author>
            <type>journals</type>
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            <pubDate>Thu, 02 Apr 2009 04:00:00 +0100</pubDate>
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            <title>Evaluation of intracellular signalling pathways in response to insulin-like growth factor I in apoptotic-resistant activated human hepatic stellate cells</title>
            <link>http://www.medworm.com/index.php?rid=2145452&amp;cid=s_38185_61_f&amp;fid=38185&amp;url=http%3A%2F%2Fwww.fibrogenesis.com%2Fcontent%2F2%2F1%2F1</link>
            <description>Conclusions:
In addition to Bcl-2, several other anti-apoptotic pathways are responsible for human hepatic stellate cell resistance to apoptosis. These features are relevant for the progression and limited reversibility of liver fibrosis in humans. (Source: Fibrogenesis and Tissue Repair)</description>
            <author>Fibrogenesis and Tissue Repair</author>
            <type>journals</type>
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            <pubDate>Fri, 30 Jan 2009 05:00:00 +0100</pubDate>
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            <title>Organotypic modelling as a means of investigating epithelial-stromal interactions during tumourigenesis</title>
            <link>http://www.medworm.com/index.php?rid=2029679&amp;cid=s_38185_61_f&amp;fid=38185&amp;url=http%3A%2F%2Fwww.fibrogenesis.com%2Fcontent%2F1%2F1%2F8</link>
            <description>The advent of co-culture approaches has allowed researchers to more accurately model the behaviour of epithelial cells in cell culture studies. The initial work on epidermal modelling allowed the development of reconstituted epidermis, growing keratinocytes on top of fibroblasts seeded in a collagen gel at an air-liquid interface to generate terminally differentiated 'skin equivalents'. In addition to developing ex vivo skin sheets for the treatment of burns victims, such cultures have also been used as a means of investigating both the development and repair of the epidermis, in more relevant conditions than simple two-dimensional culture, but without the use of animals. More recently, by varying the cell types used and adjusting the composition of the matrix components, this physiologica...</description>
            <author>Fibrogenesis and Tissue Repair</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2029679</comments>
            <pubDate>Thu, 11 Dec 2008 05:00:00 +0100</pubDate>
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            <title>Transplantation of genetically engineered cardiac fibroblasts producing recombinant human erythropoietin to repair the infarcted myocardium</title>
            <link>http://www.medworm.com/index.php?rid=2001042&amp;cid=s_38185_61_f&amp;fid=38185&amp;url=http%3A%2F%2Fwww.fibrogenesis.com%2Fcontent%2F1%2F1%2F7</link>
            <description>Conclusion:
In situ expression of rhEPO enhances vascularization and reduces cell apoptosis in the infarcted myocardium. However, local EPO therapy is insufficient for functional improvement after MI in rat. (Source: Fibrogenesis and Tissue Repair)</description>
            <author>Fibrogenesis and Tissue Repair</author>
            <type>journals</type>
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            <pubDate>Mon, 03 Nov 2008 05:00:00 +0100</pubDate>
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        <item>
            <title>Welcome to Fibrogenesis &amp; Tissue Repair</title>
            <link>http://www.medworm.com/index.php?rid=2001047&amp;cid=s_38185_61_f&amp;fid=38185&amp;url=http%3A%2F%2Fwww.fibrogenesis.com%2Fcontent%2F1%2F1%2F1</link>
            <description>Fibroproliferative diseases affecting different organs and systems constitute the largest burden and challenge of modern medicine. Nearly 45% of all deaths in the developed world are caused by chronic inflammatory and fibrogenic disorders such as cardiovascular disease, pulmonary fibrosis, progressive kidney disease, systemic sclerosis, liver cirrhosis and inflammatory bowel disease. In addition, chronic inflammation and fibrotic tissue remodelling associated with neo-angiogenesis represent key mechanisms leading to the development of cancer, thus accounting for an additional number of deaths. Regardless of the final clinical outcome, all chronic fibrogenic disorders have a major impact on the quality of life of millions of individuals worldwide and represent a major cost for public health...</description>
            <author>Fibrogenesis and Tissue Repair</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2001047</comments>
            <pubDate>Mon, 13 Oct 2008 04:00:00 +0100</pubDate>
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            <title>Viruses as co-factors for the initiation or exacerbation of lung fibrosis</title>
            <link>http://www.medworm.com/index.php?rid=2001046&amp;cid=s_38185_61_f&amp;fid=38185&amp;url=http%3A%2F%2Fwww.fibrogenesis.com%2Fcontent%2F1%2F1%2F2</link>
            <description>Idiopathic pulmonary fibrosis (IPF) remains exactly that. The disease originates from an unknown cause, and little is known about the mechanisms of pathogenesis. While the disease is likely multi-factorial, evidence is accumulating to implicate viruses as co-factors (either as initiating or exacerbating agents) of fibrotic lung disease. This review summarizes the available clinical and experimental observations that form the basis for the hypothesis that viral infections may augment fibrotic responses. We review the data suggesting a link between hepatitis C virus, adenovirus, human cytomegalovirus and, in particular, the Epstein-Barr gammaherpesvirus, in IPF. In addition, we highlight the recent associations made between gammaherpesvirus infection and lung fibrosis in horses and discuss t...</description>
            <author>Fibrogenesis and Tissue Repair</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2001046</comments>
            <pubDate>Mon, 13 Oct 2008 04:00:00 +0100</pubDate>
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            <title>Connective tissue growth factor promoter activity in normal and wounded skin</title>
            <link>http://www.medworm.com/index.php?rid=2001045&amp;cid=s_38185_61_f&amp;fid=38185&amp;url=http%3A%2F%2Fwww.fibrogenesis.com%2Fcontent%2F1%2F1%2F3</link>
            <description>In this report, we use transgenic knock-in mice in which the Pacific jellyfish Aequorea victoria enhanced green fluorescent protein (E-GFP) gene has been inserted between the endogenous CTGF promoter and gene. Unwounded (day 0) and wounded (days 3 and 7) skin was examined for GFP to detect cells in which the CTGF promoter was active, α-smooth muscle actin (α-SMA) to detect myofibroblasts, and NG2 expression to detect pericytes. In unwounded mice, CTGF expression was absent in epidermis and was present in a few cells in the dermis. Upon wounding, CTGF expression was induced in the dermis. Double immunolabeling revealed that CTGF-expressing cells also expressed α-SMA, indicating the CTGF was expressed in myofibroblasts. A subset (~30%) of myofibroblasts were also NG2 positive, indicating ...</description>
            <author>Fibrogenesis and Tissue Repair</author>
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            <pubDate>Mon, 13 Oct 2008 04:00:00 +0100</pubDate>
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            <title>Role of paracrine factors in stem and progenitor cell mediated cardiac repair and tissue fibrosis</title>
            <link>http://www.medworm.com/index.php?rid=2001044&amp;cid=s_38185_61_f&amp;fid=38185&amp;url=http%3A%2F%2Fwww.fibrogenesis.com%2Fcontent%2F1%2F1%2F4</link>
            <description>A new era has begun in the treatment of ischemic disease and heart failure. With the discovery that stem cells from diverse organs and tissues, including bone marrow, adipose tissue, umbilical cord blood, and vessel wall, have the potential to improve cardiac function beyond that of conventional pharmacological therapy comes a new field of research aiming at understanding the precise mechanisms of stem cell-mediated cardiac repair. Not only will it be important to determine the most efficacious cell population for cardiac repair, but also whether overlapping, common mechanisms exist. Increasing evidence suggests that one mechanism of action by which cells provide tissue protection and repair may involve paracrine factors, including cytokines and growth factors, released from transplanted s...</description>
            <author>Fibrogenesis and Tissue Repair</author>
            <type>journals</type>
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            <pubDate>Mon, 13 Oct 2008 04:00:00 +0100</pubDate>
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            <title>Redox mechanisms in hepatic chronic wound healing and fibrogenesis</title>
            <link>http://www.medworm.com/index.php?rid=2001043&amp;cid=s_38185_61_f&amp;fid=38185&amp;url=http%3A%2F%2Fwww.fibrogenesis.com%2Fcontent%2F1%2F1%2F5</link>
            <description>Reactive oxygen species (ROS) generated within cells or, more generally, in a tissue environment, may easily turn into a source of cell and tissue injury. Aerobic organisms have developed evolutionarily conserved mechanisms and strategies to carefully control the generation of ROS and other oxidative stress-related radical or non-radical reactive intermediates (that is, to maintain redox homeostasis), as well as to 'make use' of these molecules under physiological conditions as tools to modulate signal transduction, gene expression and cellular functional responses (that is, redox signalling). However, a derangement in redox homeostasis, resulting in sustained levels of oxidative stress and related mediators, can play a significant role in the pathogenesis of major human diseases character...</description>
            <author>Fibrogenesis and Tissue Repair</author>
            <type>journals</type>
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            <pubDate>Mon, 13 Oct 2008 04:00:00 +0100</pubDate>
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