Molecular and Cellular Basis of Cardiovascular Gender Differences

Abstract

Cardiovascular diseases (CVDs), the major cause of morbidity and mortality for both men and women, occur uncommonly in premenopausal women, but their incidence rises sharply after the menopausal transition. Cardiovascular gender differences are apparent long before CVDs appear in men and women, and improved understanding of the biology underlying these differences has the potential to advance the diagnosis and treatment of CVDs in both sexes. This review considers gender differences in the molecular and cellular physiology of the heart and blood vessels in health and disease, highlighting understudied areas that can help resolve the current controversy regarding hormone replacement therapy and improve cardiovascular health in women.

Estrogen anti-inflammatory activity in brain: A therapeutic opportunity for menopause and neurodegenerative diseases

“…However, the potent activity of exogenous estrogens in experimental models is paralleled by controversial results in humans ( [210,209]). Secondary analyses of recent randomized clinical trials, that originally raised controversies among the scientific community as to the risk/benefit ratio of HT ( [85,159,237]), helped to consolidate a novel hypothesis on the efficacy of hormone therapy [200]; it is now hypothesized that HT should be started in early menopause, as a preventative treatment of relatively healthy women, in order to avoid the negative consequences of hypoestrogenicity per se [92]. In fact, observational and randomized clinical trials show that HT does not improve memory or intellectual functions in women already affected by mild to moderate AD ( [70,172,199]), whereas it delays disease onset when administered in healthy perimenopausal women ( [100,117,200,228]).…”

Association between lipid profile and circulating concentrations of estrogens in young men

“…Consistently, estimates of phenotypic correlation between estradiol and testosterone differ across studies (22). In addition, the biological actions exerted by testosterone and estradiol on cardiovascular system are mediated by different types of receptors (23). This molecular variation may underlie differences in associations of cardiovascular phenotypes with each of these sex hormones.…”

“…Future long-term prospective studies on estrogens and cardiovascular risk factors are needed to provide a direct verification of our cross-sectional observations. Accumulated data from experimental models and clinical studies suggest that there are substantial differences in molecular mechanisms underlying estrogens actions between male and female cardiovascular system (23). This sexual dimorphism is apparent both at the biochemical (circulating levels of hormones) and cellular (expression profile of sex steroid receptors) level and may be related to sex-specific genetic mechanisms and differences in response to modulating effect of environmental factors in males and females.…”

Le paradoxe cardiovasculaire de la grossesse

“…Il est reconnu que les hormones de l'ovaire exercent des effets vasodilatateurs, ce phénomène est certes mieux documenté pour les oestrogènes que pour la progestérone (voir [23]). Ces facteurs provoquent une hausse graduelle du volume plasmatique ; et le débit cardiaque (volume d'éjection systolique et fréquence) augmente alors graduellement sans doute en réponse à cette vasodilatation pour maintenir la pression artérielle.…”