COLUMBUS, Ohio -- Researchers long believed that post-menopausal women undergoing hormone replacement therapy may also gain an added reduction in their risk of developing coronary artery disease. But when a major study released last year showed no such reduction in risk, cardiologists wondered why.
Now, a new study may reveal part of the reason: The gene that's responsible for making receptors to the hormone estrogen might be 'out of service' as a consequence of atherosclerosis, preventing the formation of the receptor. If there aren't enough of these receptors within the cells making up the arteries of the cardiovascular system, estrogen cannot provide any preventative effect.
That, at least, seems to be the explanation provided by a study by researchers from Ohio State University and Johns Hopkins Medical Institutions. Their report in the journal Cardiovascular Research blames the missing estrogen benefit on genetic changes caused by a process called DNA methylation.
Pascal Goldschmidt, professor of internal medicine and head of Ohio State's Heart and Lung Institute and its Division of Cardiology, and director of the study, said the findings may explain the results of earlier attempts to understand estrogen's role in cardiovascular disease.