Role of caveolin-eNOS platform and mitochondrial ATP-sensitive potassium channel in abrogated cardioprotective effect of ischemic preconditioning in postmenopausal women

Caveolin, the protein of the caveolar membrane, interacts and binds with endothelial nitric oxide synthase (eNOS), forming a caveolin-eNOS complex leading to suppression of the eNOS activity. Caveolin, therefore, maintains eNOS in the inactivated state leading to reduced nitric oxide (NO) production. Ischemic preconditioning disrupts the caveolin-eNOS complex leading to activation of the eNOS and thus results in cardioprotection. During ischemic preconditioning, NO produces cardioprotection by the opening of the K-ATP channel, and the caveolin forms a suitable signalling platform facilitating the interaction of NO with the K-ATP channel. Estrogen deficiency has been reported to upregulate caveolin-1 expression. The article aims to review the various mechanisms that placed the women at the risk of coronary artery diseases after postmenopausal estrogen deficiency and their role in the cardioprotective effect of ischemic preconditioning.

Automated summary

Caveolin interacts with eNOS to suppress its activity, leading to reduced NO production. Ischemic preconditioning disrupts this interaction, activating eNOS and providing cardioprotection. Estrogen deficiency upregulates Caveolin-1 expression, increasing the risk of coronary artery diseases in postmenopausal women.