These results suggest that huMSC-exos ameliorate sepsis-induced cardiomyocyte mitochondrial calcium overload via the transfer of Pink1 mRNA into cardiomyocytes to restore PINK1 expression, and upregulated PINK1 increases PKA activity to activate NCLX-mediated mCa2+ efflux and protect cardiomyocytes from injury. The gene discussed is PINK1; the disease is Sepsis.