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Updated: Jul 11, 2026

An In Vivo Estrogen Deficiency Mouse Model for Screening Exogenous Estrogen Treatments of Cardiovascular Dysfunction After Menopause
Published on: August 13, 2019
[Cardiovascular disease as a current threat of older women. Relation to estrogens]
Arturo Zárate1, Renata Saucedo, Lourdes Basurto
1Unidad de Investigación Médica de Enfemedades Endocinas, Hospital de Especialidades, Centro Médico Nacional Siglo XXI, IMSS. zaratre@att.net.mx
Insights
Cardiovascular disease (CVD) risk increases in women post-menopause due to hormonal shifts and inflammation. Hormone therapy
Area of Science:
- Cardiovascular health
- Endocrinology
- Immunology
Context:
- Cardiovascular disease (CVD) is a leading cause of death in women globally.
- Menopause is linked to increased CVD risk due to metabolic and hormonal changes.
- Declining ovarian function elevates proinflammatory cytokines, driving atherosclerosis.
Purpose:
- To explore the relationship between menopause, inflammation, and cardiovascular disease risk in women.
- To evaluate the potential cardioprotective effects of hormone therapy in postmenopausal women.
- To investigate the role of inflammation in hormone therapy's impact on cardiovascular disease.
Summary:
- Menopause-associated hormonal changes increase proinflammatory cytokines, contributing to atherosclerosis and cardiovascular disease.
- Estrogen's cardioprotective role is suggested by observational studies, but clinical trials on hormone therapy show mixed results.
- Inflammation is a key mechanism potentially mediating hormone therapy's effects on cardiovascular disease.
Impact:
- Highlights the critical role of inflammation in postmenopausal cardiovascular disease.
- Questions the universal benefit of hormone therapy for cardiovascular risk reduction in women.
- Emphasizes the need for further research into personalized cardiovascular disease prevention strategies for women.
Abstract:
Cardiovascular disease (CVD) is the leading cause of death in women around the world. Cardiovascular disease risk increases after the menopause which may be related to metabolic and hormonal changes. The decline in ovarian function with menopause is associated with spontaneous increases in proinflammatory cytokines. Chronic inflammation is a major factor that drives the progression of atherosclerosis and atherothrombosis. Measurement of the inflammatory markers has been postulated as a method of determining increased risk of cardiovascular disease in apparently healthy older women. Endogenous estrogen appears to be cardioprotective and several observational epidemiological studies have suggested that hormone therapy reduces the risk of coronary events in healthy postmenopausal women. However, recent clinical studies failed to show such beneficial effect. Among the mechanism that may account for the effects of hormone therapy on cardiovascular disease is inflammation.
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