Cardio-oncology & otherMechanistic study
Menopausal Status Associated With Docetaxel-Induced Vascular Dysfunction in Breast Cancer Patients
- Mechanistic study
- human arterial segments and ovariectomized mouse model
Authors' conclusion
TAC-induced vascular dysfunction seen in breast cancer survivors is absent in premenopausal women, likely owing to estrogen-mediated protection against oxidative stress and eNOS inhibition.
Study context
- Population
- Women with breast cancer undergoing surgery with or without prior neoadjuvant chemotherapy (TAC protocol); arterial segments from cancer-free breast tissue; ovariectomized and control female C57BL/6J mice treated with docetaxel or placebo
- Comparison
- Premenopausal vs Postmenopausal
- Outcome
- Pathophysiologic mechanisms of TAC-induced vascular dysfunction and influence of menopausal status
Main finding
As reported in the abstract
- TAC-induced endothelial dysfunction (reduced nitric oxide bioavailability) in vessels from postmenopausal women; premenopausal women protected
- Premenopausal vessels resisted TAC-induced oxidative stress: significantly lower superoxide and hydrogen peroxide production and NOX4 NADPH-oxidase expression vs postmenopausal
- No differences between premenopausal and postmenopausal women in the non-TAC groups
- TAC resulted in lower inhibitory phosphorylation of endothelial nitric oxide synthase (eNOS) at threonine-495 and reduced rho-kinase activity in premenopausal women
- In mice, docetaxel caused endothelial dysfunction, molecular changes and hypertension only in ovariectomized animals, not in age-matched nonovariectomized controls
Original publication
Menopausal Status Associated With Docetaxel-Induced Vascular Dysfunction in Breast Cancer Patients. J Am Coll Cardiol. Published 14 January 2026. doi:10.1016/j.jacc.2025.10.077
Summarised from the published abstract; every number is checked against it