Cargando…
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...
Autores principales: | , |
---|---|
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 |
_version_ | 1782128445836230656 |
---|---|
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. |
format | Text |
id | pubmed-1513067 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2006 |
publisher | The Nuclear Receptor Signaling Atlas |
record_format | MEDLINE/PubMed |
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 |
work_keys_str_mv | AT kimjinkyung estrogensignalinginthecardiovascularsystem AT levinellisr estrogensignalinginthecardiovascularsystem |