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.