JNK regulation of hepatic manifestations of the metabolic syndrome.
Nonalcoholic fatty liver disease (NAFLD) is now recognized as both an important component of the metabolic syndrome and the most prevalent liver disease in the United States. Although the mechanisms for development of steatosis and chronic liver injury in NAFLD remain unclear, recent investigations have indicated that overactivation of c-Jun N-terminal kinase (JNK) is crucial to this process. These findings, together with evidence for the involvement of JNK signaling in other manifestations of the metabolic syndrome such as obesity and insulin resistance, have suggested that JNK could be a novel therapeutic target in this disorder. This review details findings that JNK mediates lipid accumulation and cell injury in fatty liver disease and discusses the possible cellular mechanisms of JNK actions.
Czaja
Mark J
MJ
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. mark.czaja@einstein.yu.edu
D000818:Animals; D005234:Fatty Liver / Q000201:enzymology; D006801:Humans; D048031:JNK Mitogen-Activated Protein Kinases / Q000235:genetics / Q000378:metabolism*; D008099:Liver / Q000378:metabolism / Q000473:pathology; D024821:Metabolic Syndrome / Q000201:enzymology* / Q000235:genetics; D008954:Models, Biological
D048031:JNK Mitogen-Activated Protein Kinases