Apoptosis in alcoholic and nonalcoholic steatohepatitis

被引:154
作者
Feldstein, AE
Gores, GJ
机构
[1] Mayo Clin Coll Med, Dept Gastroenterol & Hepatol, Rochester, MN 55905 USA
[2] Cleveland Clin Fdn, Dept Pediat Gastroenterol, Cleveland, OH 44195 USA
[3] Cleveland Clin Fdn, Dept Cell Biol, Cleveland, OH 44195 USA
来源
FRONTIERS IN BIOSCIENCE-LANDMARK | 2005年 / 10卷
关键词
bax; lipoapoptosis; fatty acid; apoptosis; alcohol; liver; hepatocyte; review;
D O I
10.2741/1765
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Alcohol liver disease (ALD) as well as nonalcoholic fatty liver disease (NAFLD) are two of the most common forms of chronic liver disease worldwide and may progress to cirrhosis and end stage liver disease. ALD and NAFLD seem to share many pathophysiologic mechanisms with the accumulation of lipids in the liver being the first step in the development of both conditions. While mitochondrial dysfunction and production of reactive oxygen species seem to play an important role in the progression from simple steatosis to steatohepatitis in both diseases, the pathogenesis of ALD and NAFLD as it relates to tissue injury remains poorly understood. Insights into these mechanisms are of significant clinical importance because current therapies for both conditions are limited and future therapies will be predicated by an understanding of their pathogenesis. In this review we focused on the current evidence for a central role of hepatocellular apoptosis, a specific form of cell death, in the pathogenesis of ALD and NAFLD as well as the current knowledge regarding the subcellular and molecular mechanisms involve in triggering hepatocyte apoptosis in these diseases.
引用
收藏
页码:3093 / 3099
页数:7
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