title: Autophagy in nonalcoholic steatohepatitis.
abstract: Autophagy is a critical pathway for the degradation of intracellular components by lysosomes. Established functions for both macroautophagy and chaperone-mediated autophagy in hepatic lipid metabolism, insulin sensitivity and cellular injury suggest a number of potential mechanistic roles for autophagy in nonalcoholic steatohepatitis (NASH). Decreased autophagic function in particular may promote the initial development of hepatic steatosis and progression of steatosis to liver injury. Additional functions of autophagy in immune responses and carcinogenesis may also contribute to the development of NASH and its complications. The impairment in autophagy that occurs with cellular lipid accumulation, obesity and aging may therefore have an important impact on this disease, and agents to augment hepatic autophagy have therapeutic potential in NASH.
authors.affiliation: Department of Medicine, Marion Bessin Liver Research Center and Diabetes Research and Training Center, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, USA.
authors.forename: Muhammad
authors.initials: M
authors.lastname: Amir
authors.forename: Mark J
authors.initials: MJ
authors.lastname: Czaja
mesh_terms: D001343:Autophagy / Q000276:immunology*; D006528:Carcinoma, Hepatocellular / Q000276:immunology / Q000378:metabolism; D016923:Cell Death / Q000276:immunology; D005234:Fatty Liver / Q000276:immunology / Q000378:metabolism* / Q000503:physiopathology; D006801:Humans; D007249:Inflammation / Q000276:immunology / Q000378:metabolism; D007333:Insulin Resistance / Q000276:immunology; D050356:Lipid Metabolism / Q000276:immunology; D008103:Liver Cirrhosis / Q000276:immunology / Q000378:metabolism; D008113:Liver Neoplasms / Q000276:immunology / Q000378:metabolism; D065626:Non-alcoholic Fatty Liver Disease