Journal
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
Volume 318, Issue 4, Pages H820-H829Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpheart.00734.2019
Keywords
estrogen; L-type Ca2+ channel; ryanodine receptor; sarco(endo)plasmic reticulum Ca2+-ATPase; sodium-calcium exchanger
Funding
- National Natural Science Foundation of China [81461138036]
- International (regional) cooperation and exchange of NSFCRCUK-MRC [81370329]
- Priority Academic Program Development of Jiangsu Higher Education Institutions
- Natural Science Foundation of The Jiangsu Higher Education Institutes of China [17KJB180016]
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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.
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