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Estrogen signaling in the cardiovascular system

Estrogen exerts complex biological effects through the two isoforms of estrogen receptors (ERs): ERα and ERβ. Whether through alteration of gene expression or rapid, plasma membrane-localized signaling to non-transcriptional actions, estrogen-activated ERs have significant implications in cardiovasc...

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Detalles Bibliográficos
Autores principales: Kim, Jin Kyung, Levin, Ellis R.
Formato: Texto
Lenguaje:English
Publicado: The Nuclear Receptor Signaling Atlas 2006
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1513067/
https://www.ncbi.nlm.nih.gov/pubmed/16862219
http://dx.doi.org/10.1621/nrs.04013
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author Kim, Jin Kyung
Levin, Ellis R.
author_facet Kim, Jin Kyung
Levin, Ellis R.
author_sort Kim, Jin Kyung
collection PubMed
description Estrogen exerts complex biological effects through the two isoforms of estrogen receptors (ERs): ERα and ERβ. Whether through alteration of gene expression or rapid, plasma membrane-localized signaling to non-transcriptional actions, estrogen-activated ERs have significant implications in cardiovascular physiology. 17-β-estradiol (E2) generally has a protective property on the vasculature. Estrogen treatment is anti-atherogenic, protecting injured endothelial surfaces and lowering LDL oxidation in animal models. Increased NO production stimulated by E2 results in vasodilation of the coronary vascular bed, and involves rapid activation of phosphotidylinositol-3 kinase (PI3K)/Akt signaling to eNOS in carotid and femoral arteries. Both isoforms of ERs impact various vascular functions, modulating ion channel integrity, mitigating the response to arterial injury, inducing vasodilation, and preventing development of hypertension in animal models. In addition to reducing afterload by vasodilation, ERs have a direct antihypertrophic effect on the myocardium. E2-activated ERs (E2/ER) antagonize the hypertrophic pathway induced by vasoactive peptides such as angiotensin II by activating PI3K, subsequent MICIP gene expression, leading to the inhibition of calcineurin activity and the induction of hypertrophic genes. In models of ischemia-reperfusion, E2/ER is antiapoptotic for cardiomyocytes, exerting the protective actions via PI3K and p38 MAP kinases and suppressing the generation of reactive oxygen species. In sum, E2-activated ERs consistently and positively modulate multiple aspects of the cardiovascular system.
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spelling pubmed-15130672006-07-20 Estrogen signaling in the cardiovascular system Kim, Jin Kyung Levin, Ellis R. Nucl Recept Signal Perspective Estrogen exerts complex biological effects through the two isoforms of estrogen receptors (ERs): ERα and ERβ. Whether through alteration of gene expression or rapid, plasma membrane-localized signaling to non-transcriptional actions, estrogen-activated ERs have significant implications in cardiovascular physiology. 17-β-estradiol (E2) generally has a protective property on the vasculature. Estrogen treatment is anti-atherogenic, protecting injured endothelial surfaces and lowering LDL oxidation in animal models. Increased NO production stimulated by E2 results in vasodilation of the coronary vascular bed, and involves rapid activation of phosphotidylinositol-3 kinase (PI3K)/Akt signaling to eNOS in carotid and femoral arteries. Both isoforms of ERs impact various vascular functions, modulating ion channel integrity, mitigating the response to arterial injury, inducing vasodilation, and preventing development of hypertension in animal models. In addition to reducing afterload by vasodilation, ERs have a direct antihypertrophic effect on the myocardium. E2-activated ERs (E2/ER) antagonize the hypertrophic pathway induced by vasoactive peptides such as angiotensin II by activating PI3K, subsequent MICIP gene expression, leading to the inhibition of calcineurin activity and the induction of hypertrophic genes. In models of ischemia-reperfusion, E2/ER is antiapoptotic for cardiomyocytes, exerting the protective actions via PI3K and p38 MAP kinases and suppressing the generation of reactive oxygen species. In sum, E2-activated ERs consistently and positively modulate multiple aspects of the cardiovascular system. The Nuclear Receptor Signaling Atlas 2006-07-07 /pmc/articles/PMC1513067/ /pubmed/16862219 http://dx.doi.org/10.1621/nrs.04013 Text en Copyright © 2006, Kim and Levin. This is an open-access article distributed under the terms of the Creative Commons Non-Commercial Attribution License, which permits unrestricted non-commercial use distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Perspective
Kim, Jin Kyung
Levin, Ellis R.
Estrogen signaling in the cardiovascular system
title Estrogen signaling in the cardiovascular system
title_full Estrogen signaling in the cardiovascular system
title_fullStr Estrogen signaling in the cardiovascular system
title_full_unstemmed Estrogen signaling in the cardiovascular system
title_short Estrogen signaling in the cardiovascular system
title_sort estrogen signaling in the cardiovascular system
topic Perspective
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1513067/
https://www.ncbi.nlm.nih.gov/pubmed/16862219
http://dx.doi.org/10.1621/nrs.04013
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