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10.1016/j.clinre.2015.06.011

http://scihub22266oqcxt.onion/10.1016/j.clinre.2015.06.011
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C4734896!4734896!26206573
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suck abstract from ncbi

pmid26206573      Clin+Res+Hepatol+Gastroenterol 2015 ; 39 (0 1): S75-9
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  • New Therapies for Hepatic Fibrosis* #MMPMID26206573
  • Koyama Y; Brenner DA
  • Clin Res Hepatol Gastroenterol 2015[Sep]; 39 (0 1): S75-9 PMID26206573show 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.
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