期刊
ONCOGENE
卷 27, 期 -, 页码 S158-S167出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/onc.2009.53
关键词
apoptosis; autophagy; heart failure; cardiac hypertrophy; myocardial infarction
资金
- National Institutes of Health (NIH, Bethesda, MD, USA) [5P50HL077101, 2R01HL059888, 5R01HL080008, 5R01HL087871, 5P50HL077113]
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. Oncogene (2009) 27, S158-S167; doi: 10.1038/onc.2009.53
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