Jiao L1, Machuki JO1, Wu Q1, Shi M1, Fu L2, Adekunle AO1, Tao X1, Xu C1, Hu X1, Yin Z1, Sun H1.
Am J Physiol Heart Circ Physiol. 2020 Feb 21. doi: 10.1152/ajpheart.00734.2019. [Epub ahead of print]
Estrogen deficiency is considered an important factor leading to cardiovascular diseases (CVDs). Indeed, the prevalence of CVDs in postmenopausal women exceeds that of premenopausal women and men of same age. Recent research findings provide evidence that estrogen plays a pivotal role in the regulation of calcium homeostasis, and hence fine-tunes normal cardiomyocytes contraction and relaxation processes. Disruption of calcium homeostasis is closely associated with the pathological mechanism of CVDs. Thus, this article maps out and summarizes the effects and mechanisms of estrogen on calcium handing proteins in cardiac myocytes, including L-type Ca2+ channel (LTCC), sarcoplasmic reticulum (SR) Ca2+ release channel named ryanodine receptor (RyR), sarcoplasmic reticulum calcium ATPase (SERCA), and sodium-calcium exchanger (NCX). In so doing, we provide theoretical and experimental evidence for the successful design of estrogen-based prevention and treatment therapies for CVDs.