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10.1159/000445269 http://scihub22266oqcxt.onion/10.1159/000445269 C4961096!4961096!27332862     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27332862&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\27332862.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Dig+Dis 2016 ; 34 (5): 589-96 Nephropedia Template TP {{tp|p=27332862|t=2016. New Developments on the Treatment of Liver Fibrosis |pdf=|usr=}}{{27332862}} gab.com Text New Developments on the Treatment of Liver Fibrosis JO: Dig Dis http://www.kidney.de/pget.php?&tw=1&pmid=27332862 #FOAvip Liver fibrosis results from many chronic injuries, and often progresses to cirrhosis, liver failure, portal hypertension, and hepatocellular carcinoma. Liver transplantation is the only treatment available for patients with advanced stages of liver fibrosis. Therefore, new strategies for anti-fibrotic therapy are required. Various kinds of hepatocyte damage result in inflammation which leads to activation of hepatic stellate cells (HSCs), which are the major source of myofibroblasts in the liver. Myofibroblasts proliferate in response to various kinds of cytokines, chemokines, and growth factors and produce extracellular matrix proteins (ECMs), which forms the fibrous scar. Myofibroblasts undergo apoptosis and inactivation when the underlying causative etiologies are cleared. Here we describe our current knowledge of targeting the steps in HSC activation as therapeutic target for liver fibrosis. Twit Text FOAVip New Developments on the Treatment of Liver Fibrosis ????Dig Dis http://www.kidney.de/pget.php?&tw=1&pmid=27332862 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27332862 #FOAvip English Wikipedia <ref>{{Cite pmid|27332862}}</ref> New Developments on the Treatment of Liver Fibrosis #MMPMID27332862 Koyama Y; Xu J; Liu X; Brenner DA Dig Dis 2016[]; 34 (5): 589-96 PMID27332862show ga Liver fibrosis results from many chronic injuries, and often progresses to cirrhosis, liver failure, portal hypertension, and hepatocellular carcinoma. Liver transplantation is the only treatment available for patients with advanced stages of liver fibrosis. Therefore, new strategies for anti-fibrotic therapy are required. Various kinds of hepatocyte damage result in inflammation which leads to activation of hepatic stellate cells (HSCs), which are the major source of myofibroblasts in the liver. Myofibroblasts proliferate in response to various kinds of cytokines, chemokines, and growth factors and produce extracellular matrix proteins (ECMs), which forms the fibrous scar. Myofibroblasts undergo apoptosis and inactivation when the underlying causative etiologies are cleared. Here we describe our current knowledge of targeting the steps in HSC activation as therapeutic target for liver fibrosis. äNew Developments on the Treatment of Liver Fibrosis (epmc).pdf DeepDyve Pubget Overpricing