Estrogen and calcium handling proteins: new discoveries and mechanisms in cardiovascular diseases

Abstract

Estrogen deficiency is considered to be an important factor leading to cardiovascular diseases (CVDs). Indeed, the prevalence of CVDs in postmenopausal women exceeds that of premenopausal women and men of the same age. Recent research findings provide evidence that estrogen plays a pivotal role in the regulation of calcium homeostasis and therefore fine-tunes normal cardiomyocyte contraction and relaxation processes. Disruption of calcium homeostasis is closely associated with the pathological mechanism of CVDs. Thus, this paper maps out and summarizes the effects and mechanisms of estrogen on calcium handling proteins in cardiac myocytes, including L-type Ca²⁺ channel, the sarcoplasmic reticulum Ca²⁺ release channel named ryanodine receptor, sarco(endo)plasmic reticulum Ca²⁺-ATPase, and sodium-calcium exchanger. In so doing, we provide theoretical and experimental evidence for the successful design of estrogen-based prevention and treatment therapies for CVDs.

Keywords: L-type Ca2+ channel; estrogen; ryanodine receptor; sarco(endo)plasmic reticulum Ca2+-ATPase; sodium-calcium exchanger.