Non-nuclear actions of estrogen: new targets for prevention and treatment of cardiovascular disease.

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Abstract
Gender-based differences in the incidence of hypertensive and coronary artery disease, the development of atherosclerosis, and myocardial remodeling after infarction are attributable to the indirect effect of estrogen on risk factor profiles, such as cholesterol levels, glucose metabolism, and insulin levels. More recent evidence, however, suggests that activated estrogen receptor (ER) mediates signaling cascades that culminate in direct protective effects such as vasodilation, inhibition of response to vessel injury, limiting myocardial injury after infarction, and attenuating cardiac hypertrophy. Although the ER is usually thought of as a ligand-dependent transcription factor, it can also rapidly mobilize signals at the plasma membrane and in the cytoplasm. Thus, a greater understanding of ER function and regulation may lead to the development of highly specific therapeutics that mediate the prevention and treatment of cardiovascular diseases.