Fig. 7
S1R can improve endoplasmic reticulum and mitochondrial function by regulating MAM and Ca2+ concentrations. A, B MitoSOX showed that BAPTA-AM mitigates mitochondrial ROS production, whereas inhibition of S1R increased mitochondrial oxidative stress (n = 3). C, D JC-1 staining showed that inhibition of S1R decreased mitochondrial membrane potential and aggravated mitochondrial damage, whereas BAPTA-AM could restore mitochondrial membrane potential to some extent (n = 3). E Western blot showed that the addition of BAPTA-AM increased mitochondrial fusion, while the addition of S1R inhibitor BD1047 promoted mitochondrial fission. F The statistical analysis diagrams of Mfn2 and Drp1 protein expression relative to GAPDH in cardiomyocyte (n = 3). G, H Ca2+ fluorescence staining showed that inhibition of S1R increased intracellular calcium concentration, whereas the use of BAPTA-AM was effective in decreasing it (n = 3). I The statistical analysis diagrams of ER-mitochondrian distance (n = 3). J TEM showed that activation of S1R modulates MAM and increased the distance between the endoplasmic reticulum one and mitochondria, whereas inhibition of S1R enhanced mitochondrial and endoplasmic reticulum contacts. **p < 0.01; ***p < 0.005; ****p < 0.001