Nitric oxide synthase II (NOS II) gene expression correlates with atherosclerotic intimal thickening. Preventive effects of HMG-CoA reductase inhibitors

Impact of Statin Use After Heart Transplantation

“…26 Statins also downregulate the expression of growth factor genes, which are important for production of smooth muscle cells. 24,26 Our study showed that statins decreased the incidence of coronary vasculopathy and hemodynamically significant rejection episodes by 67% and 63%, respectively. Different hypotheses have been proposed to explain the potential immunomodulatory role of statins.…”

“…23 Statins downregulate nitric oxide synthase II gene expression that influences endothelial nitric oxide production. 24 In heart transplant recipients, statin also improve coronary endothelial function. 25 Through inhibition of 3-hydroxy-3-methylglutarylcoenzyme A reductase, statins decrease the synthesis of mevalonate and other prenylated proteins, farnesyl pyrophosphate and geranyl pyrophosphate, which mediate intracellular signal transduction.…”

Simvastatin Reduces Endothelial NOS: Caveolin-1 Ratio but not the Phosphorylation Status of eNOS In Vivo

“…The reason for this effect remains unknown; however, plasma homocysteine remained elevated throughout the statin treatment and hyperhomocysteinemia is well documented to cause endothelial dysfunction via separate mechanisms, including increased oxidative stress 21) and reduction in eNOS co-factors 22) . It remains unclear whether the roles of statins in the prevention of CVD are solely related to its lipidAlfon and colleagues showed reduced TC by simvastatin treatment in rabbits fed 0.5% cholesterol ＋15% coconut oil for 10 weeks 15) . In addition, Nachtigal showed that simvastatin treatment reduced TC in rabbits fed 0.4% cholesterol for 2 weeks 16) The reasons for these discrepancies remain unclear; however, it is clear from clinical studies that statin therapy can reduce TC in most cases 17,18) .…”

Induction of MCP1, CCR2, and iNOS Expression in THP-1 Macrophages by Serum of Children Late After Kawasaki Disease

“…Correspondingly, the importance of the MCP-1/CCR2 pathway in the pathogenesis of neointimal hyperplasia in cuff-induced vasculitis in mice and monkeys was recently demonstrated (41). Likewise, in a diet-induced atherosclerotic rabbit model, iNOS expression in the aorta has been found to correlate with aortic intimal thickening (22). Induction of these genes in vivo in patients with KD may thus be one of the underlying mechanisms predisposing these patients to premature atherosclerosis.…”

“…Prolonged production of nitric oxide at high levels upon iNOS induction may lead to cell injury in the vessels and may play a role in the atherosclerotic process via mechanisms relating to enhancement of oxidative stress (19,20). Indeed, iNOS expression has been demonstrated in atheromatous plaque (21) and its expression correlates with atherosclerotic intimal thickening (22).…”