Cardiac dysfunction, interstitial fibrosis, myocardial cell apoptosis, and mitochondrial damage, accompanied by autophagy and mitochondrial inhibition in streptozotocin-induced diabetes models were exacerbated by knocking out Sirt3. In contrast, SIRT3 overexpression activated autophagy and the mitochondria, inhibiting mitochondrial damage as well as cardiomyocyte apoptosis, thereby protecting cardiomyocytes in vitro (Yu et al., 2017). Here, SIRT3 is linked to diabetes mellitus.