Response by Shirakabe et al to Letter Regarding Article, “Drp1-Dependent Mitochondrial Autophagy Plays a Protective Role Against Pressure Overload–Induced Mitochondrial Dysfunction and Heart Failure”
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We thank Drs Papalia and Okonko for their interest in our work.1 Autophagy is an essential mechanism by which cells maintain the quality of proteins and organelles. Although pressure overload (PO) sequentially activates nonselective autophagy (hereafter autophagy) and mitochondria-selective autophagy (hereafter mitophagy), these autophagic activities do not last long, and mitochondrial dysfunction develops thereafter. Understanding the molecular mechanism by which autophagy and mitophagy are activated transiently but then inactivated during PO should provide a key to sustaining the level of autophagy and delaying the development of heart failure.
Drs Papalia and Okonko propose that iron-dependent mechanisms may explain the transient nature of autophagy and the consequent development of mitochondrial dysfunction. The hypothesis that suppression …