Letter by Papalia and Okonko Regarding Article, “Drp1-Dependent Mitochondrial Autophagy Plays a Protective Role Against Pressure Overload–Induced Mitochondrial Dysfunction and Heart Failure”
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To the Editor:
We read with great interest the elegant article by Shirakabe et al1 on the time course of mitochondrial autophagy after murine cardiac pressure overload induced by transverse aortic constriction. Intriguingly, they found a transient increase in mitophagy at 3 to 7 days that was paralleled by upregulated Beclin 1 expression and mitochondrial Drp1 translocation. Beyond 7 days, however, mitophagic flux was downregulated, followed by mitochondrial energetic defects that preceded cardiac systolic dysfunction and overt heart failure. Haploinsufficiency of Drp1 or treatment with Tat-Beclin 1 (a Beclin 1–derived peptide that stimulates autophagy) abolished or rescued mitophagy, …