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

G. W. Dorn, L. A. Kirshenbaum

Research output: Contribution to journalReview articlepeer-review

41 Scopus citations


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.

Original languageEnglish
Pages (from-to)S158-S167
StatePublished - Dec 2008


  • Apoptosis
  • Autop hagy
  • Cardiac hypertrophy
  • He art failure
  • Myocar dial infarction


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