Abstract
Among the known cardiovascular risk factors, high low-density lipoprotein (LDL) cholesterol and low high-density lipoprotein (HDL) cholesterol are important predictors of atherosclerotic disease. Analysis of data from observational studies initially suggested that the cardioprotective effect of estrogen was due to estrogen-induced changes in serum lipoproteins [1]. After menopause, LDL levels rise while HDL levels decline [2], thus worsening the LDL-to-HDL ratio and accelerating the development of atherosclerotic disease. Estrogen replacement results in lower levels of total cholesterol, decreased levels of LDL cholesterol, increased levels of HDL cholesterol, and increased levels of triglycerides [3,4]. Estrogen stimulates the liver to increase syntheses of VLDL which results in higher blood triglyceride levels. However, estrogen also stimulates hepatic receptor-mediated clearance of highly atherogenic LDL cholesterol. Another beneficial effect of estrogen is increased synthesis of apolipoprotein A1 and A2 which results in higher blood levels of HDL cholesterol. This effect is also due to decreased clearance of HDL cholesterol, leading to increased blood HDL levels and increased clearance of tissue cholesterol by the reverse cholesterol transport pathway.
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© 1999 Kluwer Academic Publishers and Fondazione Giovanni Lorenzini
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Sullivan, J.M. (1999). Action of Specific Estrogens on the Coronary Artery: Effects on Lipoproteins, Coagulation, and Fibrinolysis. In: Women’s Health and Menopause. Medical Science Symposia Series, vol 13. Springer, Dordrecht. https://doi.org/10.1007/978-0-585-37973-9_14
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DOI: https://doi.org/10.1007/978-0-585-37973-9_14
Publisher Name: Springer, Dordrecht
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