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Menopause

Menopause

Menopause, a natural biological process marking the end of a woman's fertility, typically occurs between the fifth and sixth decade of life. This phase is characterized by the exhaustion of the ovarian follicle pool, leading to less responsive ovaries despite the high levels of Follicle Stimulating Hormone (FSH) and Luteinizing Hormone (LH). The consequential decrease in estrogen production results in symptoms like hot flashes, heavy sweating, headaches, hair loss, muscle pains, vaginal...

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Related Experiment Video

Updated: Jan 15, 2026

An In Vivo Estrogen Deficiency Mouse Model for Screening Exogenous Estrogen Treatments of Cardiovascular Dysfunction After Menopause

An In Vivo Estrogen Deficiency Mouse Model for Screening Exogenous Estrogen Treatments of Cardiovascular Dysfunction After Menopause

Published on: August 13, 2019

Menopausal Status Associated With Docetaxel-Induced Vascular Dysfunction in Breast Cancer Patients.

Piotr Szczepaniak¹, Tomasz P Mikolajczyk¹, Ewelina Jozefczuk¹

¹Department of Internal and Agricultural Medicine, Jagiellonian University Medical College, Cracow, Poland.

Journal of the American College of Cardiology

|January 14, 2026

Summary

This summary is machine-generated.

Premenopausal women are protected from chemotherapy-induced vascular dysfunction, unlike postmenopausal women. Estrogen likely shields premenopausal women from chemotherapy

Keywords:

breast cancer chemotherapy docetaxel endothelial dysfunction menopause

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Area of Science:

Cardiovascular research
Oncology
Endocrinology

Background:

Breast cancer chemotherapy significantly elevates cardiovascular risk, especially in postmenopausal women.
Mechanisms linking menopausal status to chemotherapy-induced cardiovascular risk are unclear.
Estrogen's protective role against chemotherapy's vascular effects is investigated.

Purpose of the Study:

Elucidate mechanisms of chemotherapy-induced vascular dysfunction.
Emphasize the influence of menopausal status on these vascular effects.
Focus on docetaxel's vascular impact.

Main Methods:

Vascular function, oxidative stress, and molecular pathways assessed in breast tissue arteries from premenopausal and postmenopausal women (with/without chemotherapy).
Mechanistic studies in ovariectomized and control mice treated with docetaxel or placebo.
Evaluated nitric oxide bioavailability, oxidative stress markers, and specific molecular targets.

Main Results:

Chemotherapy induced endothelial dysfunction and reduced nitric oxide bioavailability in postmenopausal women but not premenopausal women.
Premenopausal women showed resistance to chemotherapy-induced oxidative stress and lower NOX4 expression.
Molecular analysis revealed less eNOS inhibition and rho-kinase activity in premenopausal women post-chemotherapy. Docetaxel caused dysfunction only in ovariectomized mice.

Conclusions:

Chemotherapy-induced vascular dysfunction is absent in premenopausal women.
Estrogen likely provides protection against chemotherapy's oxidative stress and endothelial nitric oxide synthase inhibition.
Menopausal status is a critical factor in chemotherapy's cardiovascular side effects.