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Estrogen-mediated mechanisms in hypertension and other cardiovascular diseases

Abstract

Cardiovascular disease (CVD) is the leading cause of death globally for men and women. Premenopausal women have a lower incidence of hypertension and other cardiovascular events than men of the same age, but diminished sex differences after menopause implicates 17-beta-estradiol (E2) as a protective agent. The cardioprotective effects of E2 are mediated by nuclear estrogen receptors (ERα and ERβ) and a G protein-coupled estrogen receptor (GPER). This review summarizes both established as well as emerging estrogen-mediated mechanisms that underlie sex differences in the vasculature during hypertension and CVD. In addition, remaining knowledge gaps inherent in the association of sex differences and E2 are identified, which may guide future clinical trials and experimental studies in this field.

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Fig. 1: The protective cardiovascular actions of estrogen are mediated by nuclear receptors ERα and ERβ as well as the membrane G protein-coupled estrogen receptor (GPER).

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Funding

This work was supported by the National Institutes of Health (HL133619 and AG071746 to SHL; HL155841 to BOO), the American Heart Association (829713 to BV; 827812 to IKD), and the Tulane Center of Excellence in Sex-Based Biology & Medicine.

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Visniauskas, B., Kilanowski-Doroh, I., Ogola, B.O. et al. Estrogen-mediated mechanisms in hypertension and other cardiovascular diseases. J Hum Hypertens 37, 609–618 (2023). https://doi.org/10.1038/s41371-022-00771-0

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