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

Oncogene volume 27, pages S158–S167 (2008)Cite this article

Abstract

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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  1. Department of Medicine, Center for Pharmacogenomics, Washington University School of Medicine, St Louis, MO, USA

    G W Dorn II

  2. Institute of Cardiovascular Sciences, St Boniface General Hospital Research Centre, University of Manitoba, Winnipeg, Manitoba, Canada

    L A Kirshenbaum

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Correspondence to G W Dorn II.

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Dorn, G., Kirshenbaum, L. Cardiac reanimation: targeting cardiomyocyte death by BNIP3 and NIX/BNIP3L. Oncogene 27 (Suppl 1), S158–S167 (2008). https://doi.org/10.1038/onc.2009.53

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