PPARGC1A and diabetic cardiomyopathy: Nevertheless, overexpression of miR-22 did attenuate oxidative stress-induced injury in diabetic cardiomyopathy [83], which may be because the deacetylation of already existing PGC-1α by SIRT1 has much more impact than the miR-22-mediated suppression of PGC-1α translation in terms of the oxidative stress regulation.