Parkin deficiency results in accumulation of abnormal mitochondria in aging myocytes

Autophagy plays a critical role in cellular quality control and is involved in removing damaged or excess organelles. Dysfunctional mitochondria are quickly cleared from the cell by autophagosomes before they can cause damage to the cell. Parkin is an E3 ubiquitin ligase that selectively ubiquitinates proteins on dysfunctional mitochondria, thereby marking those mitochondria for degradation by autophagosomes. In our recent study, we investigated the functional role of Parkin in the myocardium and discovered that Parkin is dispensable in the adult heart under normal conditions. Instead, our findings suggest that Parkin plays an important role in clearing damaged mitochondria in myocytes during stress. Here, we report that Parkin deficiency results in the accumulation of abnormal mitochondria in myocytes with age.