Aging women and their endothelium: Probing the relative role of estrogen on vasodilator function

Research output: Contribution to journalReview article

1 Citation (Scopus)

Abstract

Despite signifi-cant decreases in cardiovascular disease (CVD) mortality in the past three decades, it still remains the leading cause of death in women. Following menopause and the accompanying loss of estrogen, women experience a unique, accelerated rise in CVD risk factors. Dysfunction of the endothelium represents an important antecedent to CVD development, with rapid declines in endothelial vasodilator function reportedly taking place across the menopause transition. Importantly, the decline in endothelial function is independent of chronological age and is associated with estrogen deficiency. Estrogen-mediated effects, including increasing nitric oxide bioavailability and attenuating oxidative stress and inflammation, contribute to preserving endothelial health. This review will discuss studies that have probed the role of estrogen on endothelial vasodilator function in women at discrete stages of the menopause transition and the effects of estradiol supplementation in postmenopausal women. Estrogen receptor signaling is also an important aspect of endothelial function in women, and studies suggest that expression is reduced with both acute and prolonged estrogen deficiency. Changes in regulatory mechanisms of estrogen receptor-∝ expression as well as sensitivity to estrogen may underlie the differential effects of estrogen therapy in early (≤5 yr past final menstrual period) and late postmenopausal women (κ5 yr past final menstrual period). Lastly, this review presents potential therapeutic targets that include increasing L-arginine bioavailability and estrogen receptor activation to prevent endothelial dysfunction in postmenopausal women as a strategy for decreasing CVD mortality in this high-risk population.

Original languageEnglish (US)
Pages (from-to)H395-H404
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume317
Issue number2
DOIs
StatePublished - Aug 1 2019

Fingerprint

Vasodilator Agents
Endothelium
Estrogens
Cardiovascular Diseases
Menopause
Estrogen Receptors
Biological Availability
Postmenopause
Mortality
Arginine
Cause of Death
Estradiol
Nitric Oxide
Oxidative Stress
Inflammation
Health
Therapeutics
Population

All Science Journal Classification (ASJC) codes

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

Cite this

@article{16084d2c726446b7b5386890ca5af54c,
title = "Aging women and their endothelium: Probing the relative role of estrogen on vasodilator function",
abstract = "Despite signifi-cant decreases in cardiovascular disease (CVD) mortality in the past three decades, it still remains the leading cause of death in women. Following menopause and the accompanying loss of estrogen, women experience a unique, accelerated rise in CVD risk factors. Dysfunction of the endothelium represents an important antecedent to CVD development, with rapid declines in endothelial vasodilator function reportedly taking place across the menopause transition. Importantly, the decline in endothelial function is independent of chronological age and is associated with estrogen deficiency. Estrogen-mediated effects, including increasing nitric oxide bioavailability and attenuating oxidative stress and inflammation, contribute to preserving endothelial health. This review will discuss studies that have probed the role of estrogen on endothelial vasodilator function in women at discrete stages of the menopause transition and the effects of estradiol supplementation in postmenopausal women. Estrogen receptor signaling is also an important aspect of endothelial function in women, and studies suggest that expression is reduced with both acute and prolonged estrogen deficiency. Changes in regulatory mechanisms of estrogen receptor-∝ expression as well as sensitivity to estrogen may underlie the differential effects of estrogen therapy in early (≤5 yr past final menstrual period) and late postmenopausal women (κ5 yr past final menstrual period). Lastly, this review presents potential therapeutic targets that include increasing L-arginine bioavailability and estrogen receptor activation to prevent endothelial dysfunction in postmenopausal women as a strategy for decreasing CVD mortality in this high-risk population.",
author = "Somani, {Yasina B.} and Pawelczyk, {James Anthony} and {De Souza}, {Mary Jane} and Kris-Etherton, {Penny Margaret} and Proctor, {David Nathan}",
year = "2019",
month = "8",
day = "1",
doi = "10.1152/ajpheart.00430.2018",
language = "English (US)",
volume = "317",
pages = "H395--H404",
journal = "American Journal of Physiology",
issn = "0363-6135",
publisher = "American Physiological Society",
number = "2",

}

TY - JOUR

T1 - Aging women and their endothelium

T2 - Probing the relative role of estrogen on vasodilator function

AU - Somani, Yasina B.

AU - Pawelczyk, James Anthony

AU - De Souza, Mary Jane

AU - Kris-Etherton, Penny Margaret

AU - Proctor, David Nathan

PY - 2019/8/1

Y1 - 2019/8/1

N2 - Despite signifi-cant decreases in cardiovascular disease (CVD) mortality in the past three decades, it still remains the leading cause of death in women. Following menopause and the accompanying loss of estrogen, women experience a unique, accelerated rise in CVD risk factors. Dysfunction of the endothelium represents an important antecedent to CVD development, with rapid declines in endothelial vasodilator function reportedly taking place across the menopause transition. Importantly, the decline in endothelial function is independent of chronological age and is associated with estrogen deficiency. Estrogen-mediated effects, including increasing nitric oxide bioavailability and attenuating oxidative stress and inflammation, contribute to preserving endothelial health. This review will discuss studies that have probed the role of estrogen on endothelial vasodilator function in women at discrete stages of the menopause transition and the effects of estradiol supplementation in postmenopausal women. Estrogen receptor signaling is also an important aspect of endothelial function in women, and studies suggest that expression is reduced with both acute and prolonged estrogen deficiency. Changes in regulatory mechanisms of estrogen receptor-∝ expression as well as sensitivity to estrogen may underlie the differential effects of estrogen therapy in early (≤5 yr past final menstrual period) and late postmenopausal women (κ5 yr past final menstrual period). Lastly, this review presents potential therapeutic targets that include increasing L-arginine bioavailability and estrogen receptor activation to prevent endothelial dysfunction in postmenopausal women as a strategy for decreasing CVD mortality in this high-risk population.

AB - Despite signifi-cant decreases in cardiovascular disease (CVD) mortality in the past three decades, it still remains the leading cause of death in women. Following menopause and the accompanying loss of estrogen, women experience a unique, accelerated rise in CVD risk factors. Dysfunction of the endothelium represents an important antecedent to CVD development, with rapid declines in endothelial vasodilator function reportedly taking place across the menopause transition. Importantly, the decline in endothelial function is independent of chronological age and is associated with estrogen deficiency. Estrogen-mediated effects, including increasing nitric oxide bioavailability and attenuating oxidative stress and inflammation, contribute to preserving endothelial health. This review will discuss studies that have probed the role of estrogen on endothelial vasodilator function in women at discrete stages of the menopause transition and the effects of estradiol supplementation in postmenopausal women. Estrogen receptor signaling is also an important aspect of endothelial function in women, and studies suggest that expression is reduced with both acute and prolonged estrogen deficiency. Changes in regulatory mechanisms of estrogen receptor-∝ expression as well as sensitivity to estrogen may underlie the differential effects of estrogen therapy in early (≤5 yr past final menstrual period) and late postmenopausal women (κ5 yr past final menstrual period). Lastly, this review presents potential therapeutic targets that include increasing L-arginine bioavailability and estrogen receptor activation to prevent endothelial dysfunction in postmenopausal women as a strategy for decreasing CVD mortality in this high-risk population.

UR - http://www.scopus.com/inward/record.url?scp=85070790138&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85070790138&partnerID=8YFLogxK

U2 - 10.1152/ajpheart.00430.2018

DO - 10.1152/ajpheart.00430.2018

M3 - Review article

C2 - 31173499

AN - SCOPUS:85070790138

VL - 317

SP - H395-H404

JO - American Journal of Physiology

JF - American Journal of Physiology

SN - 0363-6135

IS - 2

ER -