Substitution of the SERCA2 Cys 674 reactive thiol accelerates atherosclerosis by inducing endoplasmic reticulum stress and inflammation.

The substitution of SERCA2 C674 thiol accelerates the development of atherosclerosis by inducing ER stress and inflammation. Our findings highlight the importance of SERCA2 C674 redox state in the context of atherosclerosis and open up a novel therapeutic strategy to combat atherosclerosis.