Protective effects of estrogen on the cardiovascular system

Mendelsohn, Michael E.

doi:10.1016/s0002-9149(02)02405-0

Cited by 966 publications

(1,163 citation statements)

References 13 publications

Supporting

Mentioning

1,051

Contrasting

Unclassified

Order By: Relevance

“…Menopause and/or an early bilateral oophorectomy play a pathological role in the development of heart disease [2,3,4]. Estrogen by itself is a critical regulator hormone for oxidative stress in that it alters serum lipid concentrations, coagulation and fibrinolytic systems, antioxidant systems and the production of other vasoactive molecules, such as nitric oxide and prostaglandins, all of which can influence the development of vascular disease [5]. It is known that sex hormones are associated with oxidative status and lipid peroxidation (LPO) [6,7,8,9].…”

Section: Introductionmentioning

confidence: 99%

Relationship between Oxidative Stress and Cardiomyopathic Changes in Ovariectomized Rats

et al. 2011

View full text Add to dashboard Cite

Objectives: Menopause has a negative effect on cardiovascular functions. However, very little is known of the overall effect of menopause on the cardiac ultrastructure or the pathophysiological basis of this. Methods: A group of 12-week-old female Sprague Dawley rats were randomly allocated to healthy control (n = 6) and ovariectomy groups (n = 6). Twelve weeks after ovariectomy, the rats’ cardiac tissues were histopathologically analyzed for determination of oxidant and antioxidant enzymes [activities of catalase (CAT), superoxide dismutase (SOD), and myeloperoxidase (MPO) and amount of glutathione (GSH) and lipid peroxidation (LPO)]. Results: When compared to the control group, the ovariectomy group showed cardiomyopathic changes. In tissue, activities of CAT (185 ± 2.4 vs. 112 ± 1.4 mmol/min/mg tissue; p < 0.05), SOD (153 ± 1.0 vs. 146 ± 0.7 mmol/min/mg tissue; p < 0.05) and MPO (19 ± 0.8 vs. 8.6 ± 0.11 µmol/min/mg tissue; p < 0.05) and LPO levels (32.1 ± 0.77 vs. 14.4 ± 0.20 nmol/g tissue; p < 0.05) were significantly increased in the ovariectomy group when compared to the control group. However, GSH levels (3.43 ± 0.02 vs. 3.73 ± 0.01 nmol/g tissue; p < 0.05) were significantly lower in the ovariectomy group when compared to the control group. Conclusion: Using an experimental animal model, we were able to demonstrate that menopause causes cardiomyopathic changes, and we propose that these changes could be mediated by oxidative stress.

show abstract

Section: Introductionmentioning

confidence: 99%

Relationship between Oxidative Stress and Cardiomyopathic Changes in Ovariectomized Rats

et al. 2011

View full text Add to dashboard Cite

show abstract

“…3 Current evidence suggests that most of these effects be mediated by ERs located both in the nucleus and on the cell membrane. Conversely, ER-independent effects of estrogen on ionic currents and membrane potential 37±40 or on LDL-cholesterol oxidation 41±43 have been reported.…”

Section: E S T R O G E N R E C E P T O R S a N D T H E V E S S E Lmentioning

confidence: 99%

“…1). 3 The aim of the present work is to integrate current knowledge with new ®ndings and put the available evidence into a novel perspective that highlights the central role for estrogen receptors (ERs) in the vascular biology of estrogen.…”

mentioning

confidence: 99%

Direct effects of estrogen on the vessel wall

2001

View full text Add to dashboard Cite

“…The incidence of coronary heart disease among women increases significantly after menopause, with loss of cardiovascular protection attributed to estrogen deficiency [8]. The primary pathological entity leading to cardiovascular mortality and morbidity is atherosclerosis.…”

Section: Introductionmentioning

confidence: 99%

Genistein Inhibits Cell Proliferation and Stimulates Apoptosis in Human Coronary Artery Endothelial Cells

Kayisli

Guzeloglu‐Kayisli²,

Güzel³

et al. 2013

Gynecol Obstet Invest

View full text Add to dashboard Cite

Background/Aims: Isoflavone genistein is a plant-derived compound structurally similar to estradiol, which behaves weakly estrogenic or anti-estrogenic in a cell- and concentration-dependent manner. Genistein has been hypothesized to have beneficial effects on vascular diseases, although the mechanism has been unclear. Here, we investigated whether genistein may play a role in atherogenesis by regulating human coronary artery endothelial cell (HCAEC) survival. Methods: HCAECs obtained from 48- to 53-year-old women (n = 3) were used and immunocytochemistry, cell proliferation assay and apoptosis assay were carried on HCAECs treated by genistein. Results: Immunocytochemistry confirmed that HCAECs in culture express predominantly ESR2. Cell proliferation assay revealed that following 72 h of genistein treatment, HCAEC proliferation decreased in a concentration-dependent (10^-10 to 10^-6M) manner compared to control (p < 0.01). The anti-proliferative effect of genistein is inhibited by estradiol. Genistein (10^-8M) also induced a time-dependent increase in the number of apoptotic HCAECs after 24-, 48- and 72-hourtreatments as detected by TUNEL and morphological analyses. Conclusion: These findings suggest that genistein acts as an anti-proliferative agent on HCAECs. The anti-proliferative and proapoptotic effects of genistein on vascular cells underlie the proposed anti-atherogenic and cardioprotective role of genistein.

show abstract

Protective effects of estrogen on the cardiovascular system

Cited by 966 publications

References 13 publications

Relationship between Oxidative Stress and Cardiomyopathic Changes in Ovariectomized Rats

Relationship between Oxidative Stress and Cardiomyopathic Changes in Ovariectomized Rats

Direct effects of estrogen on the vessel wall

Genistein Inhibits Cell Proliferation and Stimulates Apoptosis in Human Coronary Artery Endothelial Cells

Contact Info

Product

Resources

About