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Structure And Mechanisms Of Action Of HMG-CoA Reductase Inhibitors

M. Brousseau, E. Schaefer
Published 2002 · Medicine

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An elevated low density lipoprotein (LDL) cholesterol concentration is a major risk factor for the development of coronary heart disease (CHD) [1], which remains the leading cause of death in our society [2]. The efficacy of LDL reduction in the prevention of CHD has clearly been demonstrated in a number of primary and secondary intervention trials (reviewed in reference [3]). Inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, the rate-limiting enzyme in cholesterol biosynthesis, constitute the most powerful class of hypolipidemic drugs currently available. Treatment with HMG-CoA reductase inhibitors, or statins, has been shown to reduce plasma LDL cholesterol, apolipoprotein (apo) B, and triglyceride concentrations in a variety of hypercholesterolemic subjects [3, 4, 5, 6, 7, 8, 9, 10], while modestly increasing levels of high density lipoprotein (HDL) cholesterol [3].
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