RYR2 and myocardial infarction: The hyperactivation of calpain could further degrade calcium-handling and contractility-related myofilament proteins to impair cardiomyocyte contraction and activate multiple cell apoptosis pathways [47], which is concordant with our result that hiPSC-EC exosomes could improve the recovery of SERCA-2a and RyR-2 protein expression after MI.