期刊
WORLD JOURNAL OF GASTROENTEROLOGY
卷 20, 期 36, 页码 12908-12933出版社
BAISHIDENG PUBLISHING GROUP INC
DOI: 10.3748/wjg.v20.i36.12908
关键词
Alcoholic liver disease; Autophagy; Fatty liver; Lipin-1; FoxO3; RIP3; IL-22
资金
- NIAAA [R01 AA020518]
- National Center for Research Resources [5P20RR021940, T32 ES007079]
- Biomedical Research Training Program Fellowship from University of Kansas Medical Center
Alcoholic liver disease is a major health problem in the United States and worldwide. Chronic alcohol consumption can cause steatosis, inflammation, fibrosis, cirrhosis and even liver cancer. Significant progress has been made to understand key events and molecular players for the onset and progression of alcoholic liver disease from both experimental and clinical alcohol studies. No successful treatments are currently available for treating alcoholic liver disease; therefore, development of novel pathophysiological-targeted therapies is urgently needed. This review summarizes the recent progress on animal models used to study alcoholic liver disease and the detrimental factors that contribute to alcoholic liver disease pathogenesis including miRNAs, S-adenosylmethionine, Zinc deficiency, cytosolic lipin-1 beta, IRF3-mediated apoptosis, RIP3-mediated necrosis and hepcidin. In addition, we summarize emerging adaptive protective effects induced by alcohol to attenuate alcohol-induced liver pathogenesis including FoxO3, IL-22, autophagy and nuclear lipin-1 alpha.
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