Can modulation of endothelial nitric oxide synthase explain the vasculoprotective actions of statins?
Statin-based drugs are the mainstay of therapy for coronary artery disease. Recent insights into the cellular mechanisms of this class of drugs suggest that modulation of nitric oxide synthesis contributes to their beneficial actions. These effects are independent of their lipid-lowering effects and result in enhanced nitric oxide release.
Sessa
W C
WC
Yale University School of Medicine, Dept of Pharmacology, Boyer Center for Molecular Medicine, 295 Congress Avenue, New Haven, CT 06536, USA. william.sessa@yale.edu
D000818:Animals; D000924:Anticholesteremic Agents / Q000494:pharmacology*; D004730:Endothelium, Vascular / Q000187:drug effects*; D006801:Humans; D000960:Hypolipidemic Agents / Q000494:pharmacology*; D050356:Lipid Metabolism; D008148:Lovastatin / Q000031:analogs & derivatives / Q000494:pharmacology*; D008954:Models, Biological; D019001:Nitric Oxide Synthase / Q000378:metabolism*; D052250:Nitric Oxide Synthase Type III; D018384:Oxidative Stress; D011499:Protein Processing, Post-Translational; D051381:Rats
D000924:Anticholesteremic Agents; D000960:Hypolipidemic Agents; D008148:Lovastatin; C496314:NOS3 protein, human; D019001:Nitric Oxide Synthase; D052250:Nitric Oxide Synthase Type III; C496316:Nos3 protein, rat