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Estrogen's role in preventing female cardiac disease

ITHACA, N.Y. -- The role of the hormone estrogen in protecting the female heart from enlargement and ultimate failure has been partly explained by studies with genetically engineered mice, according to researchers at Cornell and Vanderbilt universities.

Authors of the report in the latest issue of Nature ( March 21, 2002), "Oestrogen protects FKBP12.6 mice from cardiac hypertrophy," used the newly developed mouse "model" for an enlarged heart muscle to help explain estrogen's important role in preventing female cardiac hypertrophy -- extreme stress on the heart that is an early sign of congestive heart failure. However, the researchers say, much more research is needed into the complex causes of heart-muscle enlargement, a condition that leads to cardiac hypertrophy.

But results of the mouse studies, they say, are clear:

o Among mice genetically engineered for a predisposition to an enlarged heart muscle, male mice develop early signs of cardiac hypertrophy similar to the potentially fatal human condition, whereas similarly engineered female transgenic mice do not.

o Unless, that is, the female mice are treated with a drug to block natural estrogen production. By being unable to produce estrogen, the female mice had the same kind of cardiac hypertrophy as did the male mice -- indicating that estrogen production protects the females but not the males.

Referring to recent evaluations of estrogen replacement therapy for postmenopausal women, Michael Kotlikoff, professor and chair of clinical sciences at Cornell, says: "This finding correlates well with epidemiological data indicating an increase in the incidence of cardiomegaly (enlargement of the heart) in women after menopause. We are hopeful that these mice will provide insight to the processes leading to cardiac enlargement and the role that estrogen plays in ameliorating this process."

In addition to Kotlikoff, whose laboratory in the College of Veterinary Medicine at Co
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Contact: Roger Segelken
hrs2@cornell.edu
607-255-9736
Cornell University News Service
22-Mar-2002


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