Atorvastatin rapidly modifies vascular redox state and improves nitric oxide bioavailability in human vessels obtained from patients with advanced atherosclerosis

書誌詳細
主要な著者:	Demosthenous, M, Antoniades, C, Paschalis, A, Tousoulis, D, Bakogiannis, C, Antonopoulos, A, Lymperiadis, D, Paleopoulos, T, Channon, K, Stefanadis, C
フォーマット:	Conference item
出版事項:	2010

Oral Atorvastatin Treatment Improves NO Bioavailability and Vascular Redox State in the Human Arterial Wall, via a Tetrahydrobiopterin-Mediated Improvement of eNOS Coupling
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RAPID, DIRECT EFFECTS OF STATIN TREATMENT ON ARTERIAL REDOX STATE AND NITRIC OXIDE BIOAVAILABILITY IN HUMAN ATHEROSCLEROSIS VIA TETRAHYDROBIOPTERIN-MEDIATED ENOS COUPLING
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Rapid, direct effects of statin treatment on arterial redox state and nitric oxide bioavailability in human atherosclerosis via tetrahydrobiopterin-mediated endothelial nitric oxide synthase coupling.
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Rapid, direct effects of statin treatment on arterial redox state and nitric oxide bioavailability in human atherosclerosis via tetrahydrobiopterin- mediated endothelial nitric oxide synthase coupling
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Novel therapeutic strategies targeting vascular redox in human atherosclerosis.
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Mechanisms regulating myocardial redox state in chronic atrial fibrillation: the role of NADPH-oxidase and uncoupled nitric oxide synthases
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Statin treatment improves vascular redox state through a tetrahydrobiopterin-mediated re-coupling of endothelial nitric oxide synthase, in human atherosclerosis
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Plasma asymmetrical-dimethyl-arginine (ADMA) as a regulator of vascular redox and nitric oxide bioavailability in human vessels
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Serum adiponectin regulates vascular O2-generation and NO bioavailability in patients with coronary atherosclerosis
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Associations Between Serum Adiponectin, Vascular O2-Generation and NO Bioavailability In Patients With Coronary Atherosclerosis
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Atorvastatin rapidly improves redox state in human vein grafts ex-vivo, by directly reducing NADPH-oxidase activity and improving eNOS coupling
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The role of adiponectin at different stages of atherosclerosis in heart failure: associations with myocardial redox state
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Atorvastatin directly improves vascular redox state by affecting eNOS coupling and NADPH-oxidase activity in human vein grafts ex-vivo
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Preoperative atorvastatin treatment rapidly improves vein graft redox state by inhibiting rac1 and NADPH oxidase activity in patients undergoing elective CABG
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Genetic variability of MTHFR affects vascular redox and nitric oxide bioavailability in human vessels, by modifying eNOS coupling
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Short-Term Atorvastatin Treatment Reduces Vascular Oxidative Stress Saphenous Vein Grafts by Improving eNOS Coupling and Reducing NADPH-Oxidase Activity in Patients Undergoing Elective CABG
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Atorvastatin Treatment for Three Days Before CABG Improves Myocardial Redox State, by Modifying NADPH-Oxidase Activity and NOS Coupling
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Myocardial Redox State Predicts Post-Operative Clinical Outcome in Patients Undergoing Elective CABG: The Role of NADPH-Oxidase and Uncoupled Nitric Oxide Synthase
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Plasma asymmetrical-dimethyl-arginine (ADMA) regulates nitric oxide bioavailability and vascular superoxide production in human vessels
著者:: Antoniades, C, 等
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Preoperative atorvastatin treatment in CABG patients rapidly improves vein graft redox state by inhibition of Rac1 and NADPH-oxidase activity.
著者:: Antoniades, C, 等
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Short-term preoperative treatment with atorvastatin improves myocardial redox state in patients undergoing elective CABG by affecting NADPH oxidase activity and NOS coupling
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Rapid Effects of Atorvastatin on Tetrahydrobiopterin-Mediated eNOS Coupling in Human Arteries, is Mediated by Stimulation of Vascular GTP-Cyclohydrolase
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Polymorphism of MTHFR gene affects vascular redox and nitric oxide bioavailability by modifying eNOS coupling
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Interrelationships between vascular superoxide and adiponectin biosynthesis in perivascular adipose tissue in human atherosclerosis
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NADPH-oxidase activity in peripheral blood mononuclear cells as a novel inflammatory marker in atherosclerosis
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Atorvastatin rapidly reduces myocardial superoxide and peroxynitrite generation in human atherosclerosis, by suppressing NADPH-oxidase activity independently of LDL lowering
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Is vascular superoxide triggering adiponectin biosynthesis in perivascular adipose tissue in patients with atherosclerosis?
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Effects of atorvastatin on endothelial function and the expression of proinflammatory cytokines and adhesion molecules in young subjects with successfully repaired coarctation of aorta.
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Effects of atorvastatin on endothelial function and the expression of proinflammatory cytokines and adhesion molecules in young subjects with successfully repaired coarctation of aorta
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Statins ameliorate atherosclerosis induced by inhibition of nitric oxide synthase: another novel vascular protective mechanism?
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MYOCARDIAL O2-AND ONOO-GENERATION IN CHRONIC ATRIAL FIBRILLATION
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Role of asymmetrical dimethylarginine in inflammation-induced endothelial dysfunction in human atherosclerosis.
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Systemic Lipid Peroxydation and Myocardial Superoxide/Peroxynitrite Anions as Predictors of Post-Operative Outcome in Cardiac Surgery
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LOCAL ADIPONECTIN SYNTHESIS IN ADIPOSE TISSUE REGULATES VASCULAR SUPEROXIDE GENERATION IN PATIENTS WITH CORONARY ATHEROSCLEROSIS: INSIGHTS BY USING FUNCTIONAL GENETIC POLYMORPHISMS OF ADIPONECTIN GENE
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Plasma asymmetrical-dimethyl-arginine affects eNOS vascular superoxide radical production and nitric oxide bioavailability in human arteries and veins
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Effects of endothelial nitric oxide synthase gene polymorphisms on oxidative stress, inflammatory status, and coronary atherosclerosis: an example of a transient phenotype.
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Systemic and local myocardial redox state as predictors of post-operative outcome in patients undergoing coronary artery bypass grafting
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Nanoparticles: a promising therapeutic approach in atherosclerosis.
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Myocardial Redox State Predicts Post-Operative Atrial Fibrillation in Cardiac Surgery
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Homocysteine and coronary atherosclerosis: from folate fortification to the recent clinical trials.
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Atorvastatin rapidly modifies vascular redox state and improves nitric oxide bioavailability in human vessels obtained from patients with advanced atherosclerosis

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