Diverse effects of statins on endothelial cells?

Abstract

T he vascular endothelium is a dynamic interface, normally providing a non-adhesive, non-thrombogenic surface for blood constituents. However, in response to proinflammatory stimuli from cytokines and bacterial products, or in response to vascular wall shear stress, induction of adhesion molecules and the expression of endothelial cell (EC) surface procoagulant proteins such as tissue factor (TF) may occur. The 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors or statins, are potent inhibitors of cholesterol synthesis in the mevalonate pathway. Clinical trials of statin therapy have demonstrated beneficial effects in primary and secondary prevention of coronary heart disease as well as ischemic stroke (1–6). Because mevalonate is a precursor of not only cholesterol, but also a variety of nonsteroidal isoprenoid compounds essential for normal cellular activity, the inhibition of HMGCoA reductase may have potential pleiotropic effects. Prenylation . . .