The PINK1-Parkin mitophagy pathway was also reported to be indispensable for normal heart function as Pink1−/− deficient mice displayed cardiac hypertrophy, increased oxidative stress, mitochondrial dysfunction, higher fibrosis and cardiomyocyte apoptosis [170], whereas Parkin deficient mice exhibited increased sensitivity to myocardial infarction, reduced survival, and impaired mitophagy associated with accumulation of swollen dysfunctional mitochondria [171]. Here, PRKN is linked to cardiac hypertrophy.