Why the study?
The cellular and molecular mechanisms underlying the loss of cardiovascular disease protection across the pre- to peri- to menopause transition remain understudied.
The transition to menopause in a murine model is associated with distinct myocardial transcriptomic and proteomic shifts related to altered cardiac energetics and adverse remodeling.
Requires human validation before informing menopausal CVD strategies; leaves open stage-specific mechanistic targets.
Cycling and perimenopausal females are protected from cardiovascular disease (CVD) whereas menopausal females are more susceptible to CVD and other pathological sequalae. The cellular and molecular mechanisms underlying loss of CVD protection across the pre- to peri- to menopause transition remain understudied. Using the murine 4-vinylcyclohexene diepoxide (VCD) model of menopause we highlight cellular and molecular signatures from hearts at each hormonally distinct stage that included transcriptomic, proteomic, and cell biological analyses.
No takes yet. Share an insight, caveat, or question.
Lopez‐Pier et al. (2025) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: