Cardiovascular disease (CVD) is the leading cause of death among women globally. Sex differences in CVD pathogenesis are well established, and female-specific risk factors, including adverse pregnancy outcomes, are increasingly recognized as CV risk factors. Premature/early menopause is an important risk factor for CVD development in women, but mechanistic insights underlying its association with CVD are limited. This knowledge gap has important clinical implications, considering that up to 10% of women undergo early menopause. In this context, we sought to investigate potential biologic pathways that may contribute to CVD development in women with premature/early menopause.