Substitution of SERCA2 Cys 674 accelerates aortic aneurysm by inducing endoplasmic reticulum stress and promoting cell apoptosis.

The irreversible oxidation of SERCA2 C674 promotes the development of aortic aneurysm by inducing ER stress and subsequent SMC apoptosis. Our study illustrates that ER stress caused by oxidative inactivation of C674 is related to the pathogenesis of aortic aneurysm. Therefore, ER stress and SERCA2 are potential therapeutic targets for treating aortic aneurysm.