Of mice and NASH – from fat to inflammation and fibrosis

The pathophysiology of non-alcoholic steatohepatitis (NASH) is complex and modulated by exogenous and genetic factors. Since only minor advances have been made in the therapy of the disease in humans, animal models are of major relevance to dissect critical pathways which regulate the development of NASH. In vivo studies with genetically altered animals (e.g. ob/ob mice) and mice fed either a methionine and choline deficient or supra-physiological (high fat and high sucrose) diets show that NASH is the result of an interplay between steatotic hepatocytes, stellate cells and the immune system. These results have been substantiated by in vitro models. We here review the current literature about murine models of NASH and describe inflammatory pathways with the potential of therapeutic intervention.

Section editors:Cord Dohrmann, Matthias Austen, Ursula Kreuzberg – DeveloGen AG, Marie-Curie-Strasse 7, 37079 Goettingen, Germany