Mitochondria and redox signaling in steatohepatitis.
Alcoholic and nonalcoholic fatty liver diseases are potentially pathological conditions that can progress to steatohepatitis, fibrosis, and cirrhosis. These conditions affect millions of people throughout the world in part through poor lifestyle choices of excess alcohol consumption, overnutrition, and lack of regular physical activity. Abnormal mitochondrial and cellular redox homeostasis has been documented in steatohepatitis and results in alterations of multiple redox-sensitive signaling cascades. Ultimately, these changes in signaling lead to altered enzyme function and transcriptional activities of proteins critical to mitochondrial and cellular function. In this article, we review the current hypotheses linking mitochondrial redox state to the overall pathophysiology of alcoholic and nonalcoholic steatohepatitis and briefly discuss the current therapeutic options under investigation.
Division of Gastroenterology and Hepatology, Department of Internal Medicine, University of Missouri, Columbia, Missouri 65212, USA.
E Matthew
EM
Morris
R Scott
RS
Rector
John P
JP
Thyfault
Jamal A
JA
Ibdah
D000818:Animals; D004734:Energy Metabolism; D005234:Fatty Liver / Q000378:metabolism*; D006706:Homeostasis; D006801:Humans; D008930:Mitochondria, Liver / Q000378:metabolism*; D010084:Oxidation-Reduction; D015398:Signal Transduction