| Literature DB >> 27332862 |
Yukinori Koyama1, Jun Xu, Xiao Liu, David A Brenner.
Abstract
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 the 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, 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.Entities:
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Year: 2016 PMID: 27332862 PMCID: PMC4961096 DOI: 10.1159/000445269
Source DB: PubMed Journal: Dig Dis ISSN: 0257-2753 Impact factor: 2.404