Conclusion
On this basis, we conclude that estrogen increased the peak sodium current through GPER. However, under pathological conditions such as stress, estrogen attenuated the increase in both of the peak sodium current and late sodium current induced by β-adrenergic overstimulation thereby conferring protection in hiPSC-CMs. GPER mediated the protective effects of estrogen on cardiomyocytes under stress state, indicating that the application of estrogen and targeting GPER may be an effective approach to treat sodium channelopathies and stress-related heart diseases. Estrogen and GPER have very important role, based on which more drugs can be developed to prevent and treat these diseases. These results are of great clinical significance as we address an important unmet clinical need to understand the role of sex hormones in caridiovacular disease.