Statins ameliorate atherosclerosis induced by inhibition of nitric oxide synthase: another novel vascular protective mechanism?
Endothelial nitric oxide synthase (eNOS), the main source of endothelium-derived nitric oxide (NO), appears to be a rational therapeutic target in atherosclerosis. The exact mechanisms regulating eNOS protein expression in human vasculature are still under intensive investigation. Recent evidence suggests that statin treatment induces the expression of eNOS in vascular endothelium, leading to a respective improvement of endothelial function. Among other mechanisms, it seems that statins increase eNOS protein levels in the vasculature, partly by up-regulating klotho protein expression. This novel observation is consistent with several lines of clinical evidence suggesting that statins have antiatherogenic effects in human vasculature, by mechanisms other than lipid-lowering.
Tousoulis
Dimitris
D
Antoniades
Charalambos
C
Stefanadis
Christodoulos
C
D050197:Atherosclerosis / Q000201:enzymology / Q000209:etiology / Q000517:prevention & control*; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors*
D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D019001:Nitric Oxide Synthase