期刊
DIGESTIVE DISEASES
卷 34, 期 5, 页码 589-596出版社
KARGER
DOI: 10.1159/000445269
关键词
Liver fibrosis; Hepatocytes; Hepatic stellate cells; Inflammation; Myofibroblasts
资金
- NIH [2 P50 AA011999, 5 P42 ES010337, 5 U01 AA021856]
- NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES [P42ES010337] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON ALCOHOL ABUSE AND ALCOHOLISM [P50AA011999, U01AA021856] Funding Source: NIH RePORTER
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. (C) 2016 S. Karger AG, Basel
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