In our present study, we found that hyperglycemia caused excessive reactive oxygen species generation through disrupting mitochondrial biogenesis (via PGC1α and TFAM), mitochondrial fusion (via MFN2), and the reactive oxygen species scavenging process (via Mn-SOD) in the ventricular tissue of mice with type 2 diabetes. Here, PPARGC1A is linked to type 2 diabetes mellitus.