Abstract
HMG CoA reductase inhibitors (statins) have been shown to be effective lipid lowering agents and are beneficial in the primary and secondary prevention of coronary heart disease. However, the overall benefits observed with statins appear to be greater than what might be expected from changes in lipid levels alone and the positive effects have only partially been reproduced with other lipid lowering drugs, suggesting effects in addition to cholesterol lowering. In experimental models, many of the cholesterol-independent effects of statins are mediated by inhibition of isoprenoids, which serve as lipid attachments for intracellular signalling molecules such as small Rho guanosine triphosphate-binding proteins, whose membrane localization and function are dependent on isoprenylation. This review summarizes the effects of statins on endothelial function and oxidative stress.
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