title: Optimized Mouse Models for Liver Fibrosis.
abstract: Fibrosis is the excessive accumulation of extracellular matrix components due to chronic injury, with collagens as predominant structural components. Liver fibrosis can progress to cirrhosis, which is characterized by a severe distortion of the delicate hepatic vascular architecture, the shunting of the blood supply away from hepatocytes and the resultant functional liver failure. Cirrhosis is associated with a highly increased morbidity and mortality and represents the major hard endpoint in clinical studies of chronic liver diseases. Moreover, cirrhosis is a strong cofactor of primary liver cancer. In vivo models are indispensable tools to study the cellular and molecular mechanisms of liver fibrosis and to develop specific antifibrotic therapies towards clinical translation. Here, we provide a detailed description of select optimized mouse models of liver fibrosis and state-of-the-art fibrosis readouts.
authors.affiliation: Institute of Translational Immunology and Research Center for Immune Therapy (FZI), University Medical Center of the Johannes Gutenberg-University Mainz, Langenbeckstraße 1, 55131, Mainz, Germany.
authors.forename: Yong Ook
authors.initials: YO
authors.lastname: Kim
authors.affiliation: Division of Gastroenterology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
authors.forename: Yury
authors.initials: Y
authors.lastname: Popov
authors.affiliation: Institute of Translational Immunology and Research Center for Immune Therapy (FZI), University Medical Center of the Johannes Gutenberg-University Mainz, Langenbeckstraße 1, 55131, Mainz, Germany. detlef.schuppan@unimedizin-mainz.de.|Division of Gastroenterology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA. detlef.schuppan@unimedizin-mainz.de.
authors.forename: Detlef
authors.initials: D
authors.lastname: Schuppan
mesh_terms: D018435:ATP Binding Cassette Transporter, Subfamily B / Q000172:deficiency / Q000235:genetics; D000818:Animals; D001391:Azo Compounds / Q000737:chemistry; D015415:Biomarkers / Q000378:metabolism; D002251:Carbon Tetrachloride; D003094:Collagen / Q000096:biosynthesis; D004195:Disease Models, Animal; D018450:Disease Progression; D005109:Extracellular Matrix / Q000378:metabolism / Q000473:pathology*; D015870:Gene Expression; D006651:Histocytochemistry / Q000379:methods*; D006801:Humans; D006909:Hydroxyproline / Q000096:biosynthesis; D008099:Liver / Q000378:metabolism / Q000473:pathology*; D008103:Liver Cirrhosis / Q000139:chemically induced / Q000378:metabolism / Q000473:pathology*; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D013853:Thioacetamide; D000097202:ATP-Binding Cassette Sub-Family B Member 4
chemical_list: D018435:ATP Binding Cassette Transporter, Subfamily B; D001391:Azo Compounds; D015415:Biomarkers; D002251:Carbon Tetrachloride; D003094:Collagen; D006909:Hydroxyproline; D013853:Thioacetamide; D000097202:ATP-Binding Cassette Sub-Family B Member 4; C009798:C.I. direct red 80
keywords: Biliary fibrosis; Carbon tetrachloride (CCL4); Cirrhosis; Collagen; Extracellular matrix (ECM); Fibrosis; Hydroxyproline (HYP); Liver fibrosis; Mdr2-knockout; Metavir staging; Panlobular fibrosis; Picrosirius Red; Thioacetamide (TAA)