2025/12/24 by Abdullah Al-Mitwalli, Rachel Rubin, Vikram Talaulikar +3 · 1 voice
Biochemistry, Genetics and Molecular Biology · Medicine · #Phosphodiesterase function and regulation #Menopause: Health Impacts and Treatments #Sexual function and dysfunction studies
paper · doi:10.1093/jsxmed/qdaf397
openalex publication_date 2025/12/24 · openalex created_date 2026/01/17 · openalex updated_date 2026/07/22
Cardiovascular disease (CVD) remains a leading cause of morbidity and mortality worldwide. Women, comprising half the population, form a significant and growing subset of individuals at elevated cardiovascular risk. Women experience a marked rise in incidence of major adverse cardiovascular events (MACE) after menopause; however, strategies to mitigate heightened risk of myocardial infarction, stroke, and heart failure remain inadequately established. Menopause is associated with ~80–90% reduction in circulating estradiol (E2) and 50% reduction in testosterone (T) levels. The increased risk of MACE in postmenopausal women (similar to aging males) is attributed to loss of hormonally mediated cardioprotection, accumulation of CVD risk factors (hypertension, diabetes, dyslipidemia, obesity, metabolic syndrome), leading to endothelial dysfunction and microvascular changes. Estrogen plays a crucial role in maintaining vascular health by promoting vasodilation, inhibiting atherosclerosis progression, and modulating lipid and glucose metabolism; thus, with estrogen decline, cardiometabolic profile shifts toward higher blood pressure, central adiposity, insulin resistance, and dyslipidemia. Gradual decline of T in aging women may have a negative effect on cardiovascular risk.1