Figure 6

Rapamycin alleviated abnormal electrophysiology in Stx12‐cKO or energy‐deficient cardiomyocytes. a) Kymograph of Ca²⁺ dynamics in cultured control (Stx12^flox/flox) cardiomyocytes, Stx12‐cKO (Stx12^flox/flox with CTnT‐Cre) cardiomyocytes and Stx12‐cKO cardiomyocytes with rapamycin treatment. Time scale bars, 0.5 s. b) Calcium dynamical curves of control and Stx12‐cKO mouse cardiomyocytes cultured in vitro, before and after rapamycin administration. c) Decay constant of Ca²⁺ in Stx12‐CKO cardiomyocytes before and after rapamycin treatment. The decay constant of Ca²⁺ dynamics significantly decreased after rapamycin treatment (Flox‐control, n = 55 curves; CKO, n = 19 curves; cKO, rapamycin, n = 23 curves; p < 0.0001). d) Calcium dynamical curves of wild‐type cardiomyocytes in vitro with or without TMRE or rapamycin treatment (WT: black, TMRE: red, TMRE + rapamycin: green). e) Comparison of Ca²⁺ amplitudes in cardiomyocytes after TMRE and rapamycin treatment. The calcium amplitude was significantly reduced after TMRE treatment, and increased after rapamycin treatment (WT, n = 20; TMRE, n = 19, p < 0.0001; TMRE + rapamycin, n = 6, p < 0.0001). f) The decaying constant τ of Ca²⁺ in cardiomyocytes with or without TMRE or rapamycin treatment. Tau was significantly increased after TMRE treatment, and decreased after rapamycin treatment (WT, n = 16; TMRE, n = 10, p < 0.0001; TMRE + rapamycin, n = 7, p = 0.004). Statistical results: **p < 0.01, ****p < 0.0001; t‐test.