Liver fibrosis is defined as excessive accumulation of extracellular matrix, and results from maladaptive wound healing processes that occur in response to chronic liver injury and inflammation. The main etiologies of liver fibrosis include nonalcoholic fatty liver disease (NAFLD), chronic viral hepatitis, as well as alcoholic and cholestatic liver disease. In patients, liver fibrosis typically develops over several decades and can progress to cirrhosis, and liver failure due to replacement of functional liver tissue with scar tissue. Additionally, advanced fibrosis and cirrhosis are associated with an increased risk for the development of hepatocellular carcinoma. On a cellular level, hepatic fibrosis is mediated by activated hepatic stellate cells, the primary fibrogenic cell type of the liver. Murine models are employed to recapitulate, understand, and therapeutically target mechanisms of fibrosis and hepatic stellate cell activation. Here, we summarize different mouse models of liver fibrosis focusing on the most commonly used models of toxic, biliary, and metabolically induced liver fibrosis, triggered by treatment with carbon tetrachloride (CCl4), thioacetamide (TAA), bile duct ligation (BDL), 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC), and high-fat diets.
Keywords: Fatty liver; Fibroblast; Hepatic stellate cell; Injury; Liver fibrosis.