In a mouse model of diabetic cardiomyopathy, Sirt3 overexpression activated deacetylation of Foxo3A and expression of Parkin, upregulated Parkin-dependent mitophagy, inhibited mitochondrial damage and apoptosis in cardiomyocytes, and played an important role in the occurrence and development of diabetic cardiomyopathy [187]. This evidence concerns the gene SIRT3 and diabetic cardiomyopathy.