Our findings revealed a loss of mitochondrial membrane potential and overt apoptosis (demonstrated by caspase-3 and TUNEL) along with downregulated levels of PGC1α and UCP-2 in STZ-induced diabetic hearts, suggesting a corroborative role of mitochondrial dysfunction and apoptosis in diabetic cardiomyopathy, as reported previously [31]. Here, CASP3 is linked to diabetic cardiomyopathy.