Key result
Targeted ablation of Bnip3 reduced periinfarct cardiomyocyte apoptosis from 11.5% to 6.7% (p=0.011) and prevented late ventricular remodeling after ischemia/reperfusion injury in mice.
Why the study?
Does targeted ablation of Bnip3 prevent ventricular remodeling and cardiomyocyte apoptosis in mice following ischemia/reperfusion injury?
Population
Mice subjected to surgical ischemia/reperfusion (IR) injury or coronary ligation, and unstressed mice
Comparison
Targeted ablation of Bnip3 (Bnip3 knockout)… vs Wild-type (WT) mice
Design
Preclinical
Follow-up
Up to 3 weeks after ischemia/reperfusion
Authors
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Caution against clinical use in MI; extends causal RCT evidence for Bnip3 inhibition in mouse post-IR remodeling.
Does targeted ablation of Bnip3 prevent ventricular remodeling and cardiomyocyte apoptosis in mice following ischemia/reperfusion injury?
Absolute Event Rate: 6.7% vs 11.5%
p-value: p=0.011
Targeted ablation of the proapoptotic gene Bnip3 reduces post-ischemic cardiomyocyte apoptosis and prevents adverse ventricular remodeling in mice, identifying it as a potential therapeutic target for post-MI heart failure.
Diwan et al. (2007) studied Myocardial infarction (ischemia/reperfusion injury). Bnip3 gene ablation vs. Wild-type (WT) mice was evaluated on Apoptosis rate in the periinfarct region at 48 hours after ischemia/reperfusion (p=0.011). Targeted ablation of Bnip3 reduced periinfarct cardiomyocyte apoptosis from 11.5% to 6.7% (p=0.011) and prevented late ventricular remodeling after ischemia/reperfusion injury in mice.
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