Review article: the pathogenesis of fibrosis in non-alcoholic steatohepatitis.
Non-alcoholic steatohepatitis has been recognized as a significant cause of end-stage liver disease and hepatic decompensation. Despite the growing interest in this condition, the molecular mechanisms underlying the development of fibrosis in this setting are only partially understood. In this article, the cellular and molecular basis of fibrosis in chronic liver disease are briefly outlined. In addition, mechanisms specifically operating in the context of fatty liver and steatohepatitis are examined, including: insulin resistance, oxidative stress, and inflammation. Finally, recent developments indicating the possible contribution of cytokines derived from adipose tissue (adipokines) to liver fibrosis is discussed.
Marra
F
F
Dipartimento di Medicina Interna, University of Florence, Florence, Italy. f.marra@dmi.unifi.it
Aleffi
S
S
Bertolani
C
C
Petrai
I
I
Vizzutti
F
F
D017667:Adipocytes / Q000378:metabolism; D002908:Chronic Disease; D016207:Cytokines / Q000032:analysis; D005234:Fatty Liver / Q000150:complications* / Q000503:physiopathology; D006505:Hepatitis / Q000150:complications* / Q000503:physiopathology; D006801:Humans; D007333:Insulin Resistance / Q000502:physiology; D008099:Liver / Q000473:pathology; D008103:Liver Cirrhosis / Q000209:etiology* / Q000503:physiopathology; D018384:Oxidative Stress / Q000502:physiology
D016207:Cytokines