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• W2401134670 abstract "The isolation of a specific competitive inhibitor of the enzyme 3hydroxy-3-methylglutaryl COA reductase from the fungus Aspergillus terreus opened the way for the development of a new family of cholesterol-lowering agents called statins. These statins ± atorvastatin, fluvastatin, lovastatin, pravastatin and simvastatin ± are all available on the Israeli market. Their mechanism of action is to target hepatocytes and reduce cholesterol production by inhibiting HMG COA reductase, a rate-controlling enzyme that converts HMGCOA to mevalonic acid, which is a precursor of cholesterol synthesis. Reduction of cholesterol synthesis in the hepatocyte upregulates hepatic low density lipoprotein receptors, leading to increased removal of plasma LDL-C, intermediate density lipoprotein and very low density lipoproteins [1,2]. Statins reduce the production of apolipoprotein B and increase hepatic apolipoprotein-B/E receptors [3]. Apart from its hypocholesterolemic action, statins have few other anti-atherogenic properties. Cholesterol-lowering by statins results in significant improvement in endothelial function, and reduces the frequency and intensity of ischemic episodes detected by 48 hour Holter monitoring [4]. The statins induce activation of the nitric oxide synthase gene in human endothelial cells [5], decrease smooth muscle growth in vitro [6], and reduce the proliferation of macrophages induced by oxidized LDL-C and its accumulation in the cells [7]. In addition, they may affect the cells' thrombus formation [8], lower the levels of C-reactive protein in the plasma [9], and eliminate the higher risk of cardiovascular events associated with this inflammatory factor. An elevated LDL-C level is the key risk factor for coronary heart disease. Primary and secondary prevention trials have shown that the use of statins to lower LDL-C levels can substantially reduce coronary events, strokes, and death from coronary heart disease [Table 1]. Clinical studies have demonstrated that statins in addition to reduction of CHD morbidity and mortality increase survival in hypercholesterolemic and normocholesterolemic subjects. The Scandinavian Simvastatin Survival Study (4S) [10] showed that reduction of cholesterol by simvastatin reduced all-cause mortality in CHD patients. In this study 4,444 CHD patients with elevated cholesterol levels of 212±310 mg/dl were treated with simvastatin for 5 years. Results showed that all-cause mortality was reduced by 30%, major coronary events by 34%, and coronary death Editorials" @default.
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• W2401134670 date "2002-06-01" @default.
• W2401134670 modified "2023-10-18" @default.
• W2401134670 title "Statins: an effective anti-atherosclerosis therapy." @default.
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