Our data suggested that inhibition of excessive oxidative stress by N-acetylcysteine (NAC), an antioxidant which has been proven by us [22–26] and others [27, 28] to be effective in attenuating oxidative stress in diabetic hearts, could restore Cav-3 expression and improve eNOS/NO signaling, which ultimately attenuate diabetic cardiomyopathy and myocardial I/R injury in diabetic rats. Here, CAV3 is linked to diabetic cardiomyopathy.