Virginia Tech scientists at the Fralin Biomedical Research Institute said on Apr. 27 that increased cardiovascular disease risk after menopause may be due not only to declining hormone levels but also to how those changes affect gene activity.
This topic is important because heart disease remains the leading cause of death for women, and rates increase significantly during and after menopause. The new research examines how declining estrogen levels can influence epigenetics, which controls when genes are activated or deactivated, possibly explaining why metabolic conditions such as diabetes also rise after menopause.
The study, published in the journal Cells, suggests a connection between estrogen loss, changes in gene regulation, and cardiovascular health. “For years, we’ve focused on estrogen loss as the primary driver of increased heart disease risk after menopause,” Sumita Mishra, senior author of the study and assistant professor at the Fralin Biomedical Research Institute at VTC, said. “What’s becoming clear is that the story is more complex. By reframing menopause-related health risks around gene regulation, this work points to new directions for future treatments that may extend beyond hormone therapy to more directly target these regulatory pathways.” The researchers note that genetic predisposition and environmental factors like diet and exercise likely interact with these pathways.
Many current interventions used for cardiometabolic diseases in postmenopausal women—including lipid-lowering therapies and glucose-lowering agents—may intersect with gene regulatory pathways influenced by estrogen. Evidence indicates these strategies can impact metabolic signaling networks as well as DNA packaging and regulation.
Mishra’s team points out a gap in knowledge: much of what is known comes from laboratory studies rather than human trials. Ongoing research will focus on understanding how metabolic and gene-regulatory pathways interact in postmenopausal health.
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Looking ahead, Mishra’s lab will continue studying how hormonal signaling interacts with molecular pathways affecting cardiometabolic health among postmenopausal women.
