Implications for chronic use of COX-2 Inhibitors in pre-menopausal women
Heart disease is less pronounced in women than in men as humans age, but this difference narrows after menopause. Some studies have shown that estrogen slows heart disease in mouse models, but the mechanism is largely unknown. Now scientists from the University of Pennsylvania School of Medicine show for the first time that in female mice protection from hardening of the arteries purported to come from higher levels of estrogen acts predominately through cyclooxygenase (COX)-2.
Garret FitzGerald, MD, Chairman of the Department of Pharmacology, and colleagues found that estrogen binds to a cell receptor that activates COX-2, which in turn ramps up the production of the prostacyclin PGI2. This biochemical provides protective benefits both by inhibiting platelet activation and by reducing oxidative stress in the circulatory system by increasing expression of an antioxidant enzyme. Earlier experiments in mice by the FitzGerald lab and others have shown that platelet activation and oxidative stress can independently hasten hardening of the arteries. The most recent findings appear in the November 18 issue of Science.
Karen Kreeger | EurekAlert!
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