Cardiac reanimation: targeting cardiomyocyte death by BNIP3 and NIX/BNIP3L

被引:0
|
作者
G W Dorn
L A Kirshenbaum
机构
[1] Center for Pharmacogenomics,Department of Medicine
[2] Washington University School of Medicine,undefined
[3] Institute of Cardiovascular Sciences,undefined
[4] St Boniface General Hospital Research Centre,undefined
[5] University of Manitoba,undefined
来源
Oncogene | 2008年 / 27卷
关键词
apoptosis; autophagy; heart failure; cardiac hypertrophy; myocardial infarction;
D O I
暂无
中图分类号
学科分类号
摘要
Programmed cardiac myocyte death contributes to pathological ventricular remodeling and the progression of myocardial infarction or pressure overload hypertrophy to dilated cardiomyopathy. Recent work has identified importance of stress-mediated transcriptional induction of BNIP3 (BCL2 and 19-kDa interacting protein-3) and NIX/BNIP3L in cardiac remodeling. Here, the regulatory mechanisms for these two factors in the heart and their effects on programmed cardiomyocyte death are reviewed, with a focus on information derived from studies using mouse models of cardiac BNIP3 and NIX/BNIP3L overexpression and gene ablation.
引用
收藏
页码:S158 / S167
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