title: New therapies for hepatic fibrosis.
abstract: 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.
authors.affiliation: School of Medicine, University of California, San Diego, 9500 Gilman Drive, La Jolla, 92093 California, United States.
authors.forename: Yukinori
authors.initials: Y
authors.lastname: Koyama
authors.affiliation: School of Medicine, University of California, San Diego, 9500 Gilman Drive, La Jolla, 92093 California, United States. Electronic address: dbrenner@ucsd.edu.
authors.forename: David A
authors.initials: DA
authors.lastname: Brenner
mesh_terms: D017209:Apoptosis; D049109:Cell Proliferation / Q000502:physiology; D055166:Hepatic Stellate Cells / Q000473:pathology; D006801:Humans; D008099:Liver / Q000166:cytology; D008103:Liver Cirrhosis / Q000473:pathology*; D058628:Myofibroblasts / Q000502:physiology; D017382:Reactive Oxygen Species / Q000378:metabolism; D000683:Serum Amyloid P-Component / Q000502:physiology
chemical_list: D017382:Reactive Oxygen Species; D000683:Serum Amyloid P-Component