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.
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页码：S158 / S167
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