Abstract
The increasing use of 3-hydroxy-3-methylglutaryl (HMG)-CoA reductase inhibitors (statins) has revealed beneficial effects that are independent of their intended lipid-lowering effects. Understanding the mechanisms of how statins facilitate these effects may help extend their indications in both cardiovascular and noncardiovascular diseases and perhaps lead to the development of additional novel pharmaceuticals. Owing to their structural similarity with HMG-CoA, statins are able to competitively inhibit HMG-CoA reductase, the rate-limiting enzyme in cholesterol synthesis. The consequence of this inhibition is a reduction in cholesterol synthesis and subsequent secretion of ApoB-containing lipoproteins and an increase in the clearance of LDL-cholesterol through the upregulation of the
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