title: Molecular pathogenesis of liver fibrosis.
abstract: Hepatic fibrosis is the final common pathway for most chronic liver diseases. The cell responsible for hepatic fibrosis appears to be the activated myofibroblast. The myofibroblast may be derived from quiescent hepatic stellate cells, epithelial to mesenhymal transition, or derived from bone marrow precursors. Studies in primary cultures of myofibroblasts and in mouse models of hepatic fibrosis have revealed several common pathophysiological mechanisms. Hepatic fibrosis is strongly associated with oxidative stress, increased transforming growth factor beta, hepatocyte death, and chronic inflammation. Finally, the reversal of fibrosis depends upon the elimination of the activated myofibroblast.
authors.affiliation: 1318 Biomedical Sciences Building, UC San Diego Health Sciences, 9500 Gilman Drive, La Jolla, CA 92093-0602, USA. dbrenner@ucsd.edu
authors.forename: David A
authors.initials: DA
authors.lastname: Brenner
mesh_terms: D000818:Animals; D017209:Apoptosis; D005347:Fibroblasts / Q000473:pathology / Q000502:physiology; D055166:Hepatic Stellate Cells / Q000473:pathology / Q000502:physiology; D006801:Humans; D018836:Inflammation Mediators / Q000502:physiology; D008103:Liver Cirrhosis / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D051379:Mice; D018384:Oxidative Stress; D016212:Transforming Growth Factor beta / Q000502:physiology
chemical_list: D018836:Inflammation Mediators; D016212:Transforming Growth Factor beta