Key Results
Isoproterenol-induced stress increased peak sodium current and late sodium current, and shortened action potential duration but the effects of stress were eliminated by β-Estradiol. Pearson Correlation analysis demonstrated no association between estrogenic effects on sodium currents versus content of sodium channel. Activation of GPER produced similar effects as β-Estradiol, while inhibition of GPER cancelled the effects induced by β-Estradiol.
Conclusion and Implications
Estrogen through its rapid signal receptor GPER ameliorated the detrimental effects of β-adrenergic overstimulation like in cardiac stress on sodium channel dysfunction in hiPSC-CMs. These results are of great clinical significance as we need to understand the role of sex hormones in cardiovascular disease.