<?xml version="1.0" encoding="UTF-8"?>
<!-- generator="FeedCreator 1.7.2" -->
<rss version="2.0">
    <channel>
        <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>Sat, 06 Mar 2010 16:02:18 +0100</lastBuildDate>
        <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>
            <guid isPermaLink="false">2988345</guid>        </item>
        <item>
            <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>
        <comments>http://www.medworm.com/rss/comments.php?id=2831485</comments>
            <pubDate>Thu, 24 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2831485</guid>        </item>
        <item>
            <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>
        <comments>http://www.medworm.com/rss/comments.php?id=2323435</comments>
            <pubDate>Thu, 02 Apr 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2323435</guid>        </item>
        <item>
            <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>
        <comments>http://www.medworm.com/rss/comments.php?id=2145452</comments>
            <pubDate>Fri, 30 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2145452</guid>        </item>
        <item>
            <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>
            <guid isPermaLink="false">2029679</guid>        </item>
        <item>
            <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>
        <comments>http://www.medworm.com/rss/comments.php?id=2001042</comments>
            <pubDate>Mon, 03 Nov 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2001042</guid>        </item>
        <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>
            <guid isPermaLink="false">2001047</guid>        </item>
        <item>
            <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>
            <guid isPermaLink="false">2001046</guid>        </item>
        <item>
            <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>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2001045</comments>
            <pubDate>Mon, 13 Oct 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2001045</guid>        </item>
        <item>
            <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>
        <comments>http://www.medworm.com/rss/comments.php?id=2001044</comments>
            <pubDate>Mon, 13 Oct 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2001044</guid>        </item>
        <item>
            <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>
        <comments>http://www.medworm.com/rss/comments.php?id=2001043</comments>
            <pubDate>Mon, 13 Oct 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2001043</guid>        </item>
    </channel>
</rss>
