Mechanisms of lipoapoptosis: Implications for human heart disease

被引:102
作者
Listenberger, LL
Schaffer, JE
机构
[1] Washington Univ, Sch Med, Dept Internal Med, Cardiovasc Res Ctr, St Louis, MO 63110 USA
[2] Washington Univ, Sch Med, Dept Mol Biol & Pharmacol, Cardiovasc Res Ctr, St Louis, MO 63110 USA
关键词
D O I
10.1016/S1050-1738(02)00152-4
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Accumulation of long-chain fatty acids in the heart has been proposed to play a role in the development of heart failure and diabetic cardiomyopathy. Several animal models with increased cardiomyocyte lipid accumulation suggest a link between the accumulation of lipid, cardiomyocyte cell death and the development of cardiomyopathy. In this review, we discuss the mechanism through which fatty acid accumulation may contribute to the development or progression of heart failure by initiation of apoptotic cell death. Long-chain saturated fatty acids induce apoptosis through a mechanism involving the generation of reactive intermediates. Reactive intermediate production occurs in concert with de novo ceramide synthesis, but ceramide production is not required for cell death. Cardiomyocyte dysfunction and death from reactive intermediates generated by long-chain saturated fatty acids may contribute to the pathogenesis of human heart disease. (C) 2002, Elsevier Science Inc.
引用
收藏
页码:134 / 138
页数:5
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