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The Impact of Estrogen Receptor in Cardiovascular Disease
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The Impact of Estrogen Receptor in Cardiovascular Disease

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: closed (30 September 2020) | Viewed by 41629

Special Issue Editor

Prof. Dr. Antonio Cano

E-Mail Website
Guest Editor
1. Research Unit on Women’s Health—Institute of Health Research INCLIVA, 46010 Valencia, Spain
2. Department of Pediatrics, Obstetrics and Gynecology, University of Valencia, 46010 Valencia, Spain
Interests: reproductive endocrinology; hormonal action; cardiovascular disease

Special Issue Information

Dear Colleagues,

Estrogen receptors are found in the vascular wall, and experimental and clinical models show that estrogens have healthy effects on the vasculature. The NIH-based Women’s Health Initiative study found an increase in the risk of cardiovascular events in women taking menopausal hormone therapy. Several studies suggest that estrogens may trigger the rupture of advanced atherosclerotic plaques, but protect against atherosclerosis in younger, healthier arteries. The implications are huge for symptomatic early postmenopausal women. Interest has also arisen regarding potential long-term protection against an array of diseases linked with the cardiovascular tree, central nervous system, and others. This Special Issue focuses on molecular mechanisms of the impact of estrogen receptors in cardiovascular disease. We warmly welcome submissions, including original papers and reviews, on the topic of discussion.

Prof. Antonio Cano
Guest Editor

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Published Papers (4 papers)

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Review

51 pages, 2858 KiB  
Review
Estrogen Receptors and Estrogen-Induced Uterine Vasodilation in Pregnancy
by Jin Bai, Qian-Rong Qi, Yan Li, Robert Day, Josh Makhoul, Ronald R. Magness and Dong-bao Chen
Int. J. Mol. Sci. 2020, 21(12), 4349; https://doi.org/10.3390/ijms21124349 - 18 Jun 2020
Cited by 46 | Viewed by 10639
Abstract
Normal pregnancy is associated with dramatic increases in uterine blood flow to facilitate the bidirectional maternal–fetal exchanges of respiratory gases and to provide sole nutrient support for fetal growth and survival. The mechanism(s) underlying pregnancy-associated uterine vasodilation remain incompletely understood, but this is [...] Read more.
Normal pregnancy is associated with dramatic increases in uterine blood flow to facilitate the bidirectional maternal–fetal exchanges of respiratory gases and to provide sole nutrient support for fetal growth and survival. The mechanism(s) underlying pregnancy-associated uterine vasodilation remain incompletely understood, but this is associated with elevated estrogens, which stimulate specific estrogen receptor (ER)-dependent vasodilator production in the uterine artery (UA). The classical ERs (ERα and ERβ) and the plasma-bound G protein-coupled ER (GPR30/GPER) are expressed in UA endothelial cells and smooth muscle cells, mediating the vasodilatory effects of estrogens through genomic and/or nongenomic pathways that are likely epigenetically modified. The activation of these three ERs by estrogens enhances the endothelial production of nitric oxide (NO), which has been shown to play a key role in uterine vasodilation during pregnancy. However, the local blockade of NO biosynthesis only partially attenuates estrogen-induced and pregnancy-associated uterine vasodilation, suggesting that mechanisms other than NO exist to mediate uterine vasodilation. In this review, we summarize the literature on the role of NO in ER-mediated mechanisms controlling estrogen-induced and pregnancy-associated uterine vasodilation and our recent work on a “new” UA vasodilator hydrogen sulfide (H2S) that has dramatically changed our view of how estrogens regulate uterine vasodilation in pregnancy. Full article
(This article belongs to the Special Issue The Impact of Estrogen Receptor in Cardiovascular Disease)
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26 pages, 1404 KiB  
Review
The Role of Estrogen Receptors in Cardiovascular Disease
by Laila Aryan, David Younessi, Michael Zargari, Somanshu Banerjee, Jacqueline Agopian, Shadie Rahman, Reza Borna, Gregoire Ruffenach, Soban Umar and Mansoureh Eghbali
Int. J. Mol. Sci. 2020, 21(12), 4314; https://doi.org/10.3390/ijms21124314 - 17 Jun 2020
Cited by 103 | Viewed by 12580
Abstract
Cardiovascular Diseases (CVDs) are the leading cause of death globally. More than 17 million people die worldwide from CVD per year. There is considerable evidence suggesting that estrogen modulates cardiovascular physiology and function in both health and disease, and that it could potentially [...] Read more.
Cardiovascular Diseases (CVDs) are the leading cause of death globally. More than 17 million people die worldwide from CVD per year. There is considerable evidence suggesting that estrogen modulates cardiovascular physiology and function in both health and disease, and that it could potentially serve as a cardioprotective agent. The effects of estrogen on cardiovascular function are mediated by nuclear and membrane estrogen receptors (ERs), including estrogen receptor alpha (ERα), estrogen receptor beta (ERβ), and G-protein-coupled ER (GPR30 or GPER). Receptor binding in turn confers pleiotropic effects through both genomic and non-genomic signaling to maintain cardiovascular homeostasis. Each ER has been implicated in multiple pre-clinical cardiovascular disease models. This review will discuss current reports on the underlying molecular mechanisms of the ERs in regulating vascular pathology, with a special emphasis on hypertension, pulmonary hypertension, and atherosclerosis, as well as in regulating cardiac pathology, with a particular emphasis on ischemia/reperfusion injury, heart failure with reduced ejection fraction, and heart failure with preserved ejection fraction. Full article
(This article belongs to the Special Issue The Impact of Estrogen Receptor in Cardiovascular Disease)
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21 pages, 1740 KiB  
Review
The Impact of Estrogen Receptor in Arterial and Lymphatic Vascular Diseases
by Coralie Fontaine, Florent Morfoisse, Florence Tatin, Audrey Zamora, Rana Zahreddine, Daniel Henrion, Jean-François Arnal, Françoise Lenfant and Barbara Garmy-Susini
Int. J. Mol. Sci. 2020, 21(9), 3244; https://doi.org/10.3390/ijms21093244 - 4 May 2020
Cited by 24 | Viewed by 4731
Abstract
The lower incidence of cardiovascular diseases in pre-menopausal women compared to men is well-known documented. This protection has been largely attributed to the protective effect of estrogens, which exert many beneficial effects against arterial diseases, including vasodilatation, acceleration of healing in response to [...] Read more.
The lower incidence of cardiovascular diseases in pre-menopausal women compared to men is well-known documented. This protection has been largely attributed to the protective effect of estrogens, which exert many beneficial effects against arterial diseases, including vasodilatation, acceleration of healing in response to arterial injury, arterial collateral growth and atheroprotection. More recently, with the visualization of the lymphatic vessels, the impact of estrogens on lymphedema and lymphatic diseases started to be elucidated. These estrogenic effects are mediated not only by the classic nuclear/genomic actions via the specific estrogen receptor (ER) α and β, but also by rapid extra-nuclear membrane-initiated steroid signaling (MISS). The ERs are expressed by endothelial, lymphatic and smooth muscle cells in the different vessels. In this review, we will summarize the complex vascular effects of estrogens and selective estrogen receptor modulators (SERMs) that have been described using different transgenic mouse models with selective loss of ERα function and numerous animal models of vascular and lymphatic diseases. Full article
(This article belongs to the Special Issue The Impact of Estrogen Receptor in Cardiovascular Disease)
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18 pages, 656 KiB  
Review
Influence of Estrogens on Uterine Vascular Adaptation in Normal and Preeclamptic Pregnancies
by Maurizio Mandalà
Int. J. Mol. Sci. 2020, 21(7), 2592; https://doi.org/10.3390/ijms21072592 - 8 Apr 2020
Cited by 35 | Viewed by 12977
Abstract
During pregnancy, the maternal cardiovascular system undergoes significant changes, including increased heart rate, cardiac output, plasma volume, and uteroplacental blood flow (UPBF) that are required for a successful pregnancy outcome. The increased UPBF is secondary to profound circumferential growth that extends from the [...] Read more.
During pregnancy, the maternal cardiovascular system undergoes significant changes, including increased heart rate, cardiac output, plasma volume, and uteroplacental blood flow (UPBF) that are required for a successful pregnancy outcome. The increased UPBF is secondary to profound circumferential growth that extends from the downstream small spiral arteries to the upstream conduit main uterine artery. Although some of the mechanisms underlying uterine vascular remodeling are, in part, known, the factors that drive the remodeling are less clear. That higher circulating levels of estrogens are positively correlated with gestational uterine vascular remodeling suggests their involvement in this process. Estrogens binding to the estrogen receptors expressed in cytotrophoblast cells and in the uterine artery wall stimulate an outward hypertrophic remodeling of uterine vasculature. In preeclampsia, generally lower concentrations of estrogens limit the proper uterine remodeling, thereby reducing UPBF increases and restricting the growth of the fetus. This review aims to report estrogenic regulation of the maternal uterine circulatory adaptation in physiological and pathological pregnancy that favors vasodilation, and to consider the underlying molecular mechanisms by which estrogens regulate uteroplacental hemodynamics. Full article
(This article belongs to the Special Issue The Impact of Estrogen Receptor in Cardiovascular Disease)
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