Data from: Elucidation of molecular mechanisms of sex-based arrhythmias

Notably, female sex is a key element in up to 70% prevalence of drug-induced acquired LQTS, However, fundamental molecular mechanisms that explain this phenomenon are not well understood. Previous experimental and clinical studies suggested that it is likely related to differential levels of sex hormones (estradiol, progesterone and testosterone) playing opposite roles in pro-arrhythmia proclivities, exacerbating or mitigating effects of mutations or drugs on cardiac ion channels.

In the American Heart Association (AHA) sponsored career development award 19CDA34770101 "Elucidation of molecular mechanisms of sex-based arrhythmias" we focused on hormone interactions with the human Kv11.1 potassium channel (encoded by the hERG - human Ether-à-go-go-Related Gene), a major contributor to cardiac action potential repolarization and an anti-target for diverse drug molecules. We performed a comprehensive set of in silico atomistic modeling and simulations on hERG structure and function modulation by sex hormones in combination with hERG channel blockers with different proclivities for arrhythmogenesis.