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

G. W. Dorn; L. A. Kirshenbaum

doi:10.1038/onc.2009.53

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

G. W. Dorn, L. A. Kirshenbaum

Research output: Contribution to journal › Review article › peer-review

47 Scopus citations

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.

Original language	English
Pages (from-to)	S158-S167
Journal	Oncogene
Volume	27
DOIs	https://doi.org/10.1038/onc.2009.53
State	Published - Dec 2008

Keywords

Apoptosis
Autop hagy
Cardiac hypertrophy
He art failure
Myocar dial infarction

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10.1038/onc.2009.53

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title = "Cardiac reanimation: Targeting cardiomyocyte death by BNIP3 and NIX/BNIP3L",

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.",

keywords = "Apoptosis, Autop hagy, Cardiac hypertrophy, He art failure, Myocar dial infarction",

author = "Dorn, {G. W.} and Kirshenbaum, {L. A.}",

note = "Funding Information: GW Dorn is currently receiving grant support from the National Institutes of Health (NIH, Bethesda, MD, USA) (5P50HL077101; 2R01HL059888; 5R01HL080008; 5R01HL087871; 5P50HL077113). LA Kirschenbaum holds a patent for the NIP3 family of proteins (US patent no. 7, 452,869B2).",

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AU - Dorn, G. W.

AU - Kirshenbaum, L. A.

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AB - 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.

KW - Apoptosis

KW - Autop hagy

KW - Cardiac hypertrophy

KW - He art failure

KW - Myocar dial infarction

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JF - Oncogene

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

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Keywords

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