title: Mouse models of liver fibrosis.
abstract: Liver fibrosis is the final common pathway in a variety of liver diseases. To model liver fibrosis in mice is important as mechanisms not only of fibrogenesis, but also of fibrolysis, need to be clearly defined. Also, small rodents present a possibility to test potential treatments in vivo. Today, there are several mouse models of liver fibrosis available--induced by administration of hepatotoxins, by bile duct ligation or by immunological mechanisms--and, more and more widespread, transgenic animal models elucidating pathogenesis and common pathways in liver fibrosis. These different mouse models are complementary as they represent different pathways to fibrosis--as also seen in human disease. Recently, several promising treatment methods interfering with cytokine signaling have been published, offering new potential therapeutic interventions. This review seeks to summarize the different methods of fibrosis induction as well as to briefly review some promising new treatment options for fibrosis in the mouse model.
authors.affiliation: I. Department of Medicine, University Medical Centre Hamburg-Eppendorf, Hamburg, Germany.
authors.forename: C
authors.initials: C
authors.lastname: Weiler-Normann
authors.forename: J
authors.initials: J
authors.lastname: Herkel
authors.forename: A W
authors.initials: AW
authors.lastname: Lohse
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use*; D002251:Carbon Tetrachloride; D016207:Cytokines / Q000235:genetics / Q000378:metabolism*; D004195:Disease Models, Animal; D008103:Liver Cirrhosis / Q000188:drug therapy* / Q000503:physiopathology*; D051379:Mice; D018345:Mice, Knockout; D008822:Mice, Transgenic
chemical_list: D000893:Anti-Inflammatory Agents; D016207:Cytokines; D002251:Carbon Tetrachloride