As an upstream regulator of PERK, the silencing of MFN2 can prevent mitochondrial Ca2+ overload-mediated mitochondrial dysfunction, thereby reducing ER stress-mediated myocardial apoptosis [86].In addition, the lack of A-kinase anchoring protein 1 (AKAP1) in DCM impairs mitochondrial respiratory function and enhances the production of ROS, leading to increased apoptosis of myocardial cells [101]. Here, AKAP1 is linked to familial dilated cardiomyopathy.