This mechanism entailed enhanced nitration of caveolin-3 at tyrosine 73 by peroxinitrite formed from increased NADPH oxidase-induced ROS and increased iNOS-induced NO, thereby disruption the Cav3 signalosome needed for insulin sensitivity, resistance to myocardial ischemia, and several cardioprotective signaling pathways [105]. Here, CAV3 is linked to myocardial ischemia.