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10.1016/j.clinre.2015.06.011 http://scihub22266oqcxt.onion/10.1016/j.clinre.2015.06.011 C4734896!4734896 !26206573     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26206573 &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\26206573 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Clin+Res+Hepatol+Gastroenterol 2015 ; 39 Suppl 1 (0 1 ): S75-9 Nephropedia Template TP {{tp|p=26206573 |t=2015. New therapies for hepatic fibrosis |pdf=|usr=}}{{26206573 }} gab.com Text New therapies for hepatic fibrosis JO: Clin Res Hepatol Gastroenterol http://www.kidney.de/pget.php?&tw=1&pmid=26206573 #FOAvip Liver fibrosis is an outcome of many chronic diseases, and often results in cirrhosis, liver failure, and portal hypertension. Liver transplantation is the only treatment available for patients with advanced stages of liver cirrhosis. Therefore, alternative methods are required to develop new strategies for anti-fibrotic therapy. Various kinds of hepatocyte injuries cause inflammatory reactions, which lead to activation of hepatic stellate cells (HSCs). Continuous liver injuries maintain these activated HSCs, and they are called as myofibroblasts. Myofibroblasts proliferate in response to various kinds of cytokines and produce extracellular matrix proteins (ECMs). Myofibroblasts undergo apoptosis and inactivation when the underlying causative etiologies are cleared. Here, we describe the current knowledge of targeting the activated HSCs as a therapeutic target for liver fibrosis. Twit Text FOAVip New therapies for hepatic fibrosis ????Clin Res Hepatol Gastroenterol http://www.kidney.de/pget.php?&tw=1&pmid=26206573 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26206573 #FOAvip English Wikipedia <ref>{{Cite pmid|26206573 }}</ref> New therapies for hepatic fibrosis #MMPMID26206573 Koyama Y ; Brenner DA Clin Res Hepatol Gastroenterol 2015[Sep]; 39 Suppl 1 (0 1 ): S75-9 PMID26206573 show ga Liver fibrosis is an outcome of many chronic diseases, and often results in cirrhosis, liver failure, and portal hypertension. Liver transplantation is the only treatment available for patients with advanced stages of liver cirrhosis. Therefore, alternative methods are required to develop new strategies for anti-fibrotic therapy. Various kinds of hepatocyte injuries cause inflammatory reactions, which lead to activation of hepatic stellate cells (HSCs). Continuous liver injuries maintain these activated HSCs, and they are called as myofibroblasts. Myofibroblasts proliferate in response to various kinds of cytokines and produce extracellular matrix proteins (ECMs). Myofibroblasts undergo apoptosis and inactivation when the underlying causative etiologies are cleared. Here, we describe the current knowledge of targeting the activated HSCs as a therapeutic target for liver fibrosis. |Apoptosis [MESH] |Cell Proliferation/physiology [MESH] |Hepatic Stellate Cells/pathology [MESH] |Humans [MESH] |Liver Cirrhosis/*pathology [MESH] |Liver/cytology [MESH] |Myofibroblasts/physiology [MESH] |Reactive Oxygen Species/metabolism [MESH]New therapies for hepatic fibrosis (epmc).pdf DeepDyve Pubget Overpricing