Polymorphism of MTHFR gene affects vascular redox and nitric oxide bioavailability by modifying eNOS coupling

Bibliographic Details
Main Authors:	Antoniades, C, Shirodaria, C, Leeson, P, Van-Assche, T, Ratnatunga, C, Pillai, R, Tousoulis, D, Stefanadis, C, Refsurn, H, Channon, K
Format:	Conference item
Published:	2008

Genetic variability of MTHFR affects vascular redox and nitric oxide bioavailability in human vessels, by modifying eNOS coupling
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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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Genetic Polymorphism On Methyl-Tetrahydrofolate-Reductase Affects Vascular Superoxide Generation and Nitric Oxide Bioavailability By Regulating eNOS Coupling in Human Arteries and Veins
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The common genetic polymorphism C677T of methyltetrahydrofolate reductase regulates nitric oxide bioavailability and vascular superoxide production via modulation of eNOS coupling in human vessels
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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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MTHFR 677 C>T Polymorphism reveals functional importance for 5-methyltetrahydrofolate, not homocysteine, in regulation of vascular redox state and endothelial function in human atherosclerosis.
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Genetic Variability of Methyl-Tetrahydrofolate-Reductase Modifies eNOS Coupling in Human Arteries and Veins: Effects on Vascular Superoxide Generation and Nitric Oxide Bioavailabllity
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5-methyl-tetrahydrofolic acid increases nitric oxide bioavailability and decreases superoxide production by improving eNOS coupling in human vessels in vivo: Effects on intracellular tetrahydrobiopterin oxidation
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5-methyl-tetrahydrofolate increases nitric oxide bioavailability and decreases superoxide production by improving eNOS coupling and preventing the intracellular oxidation of tetrahy-drobiopterin, in human vessels in vivo
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Chronic treatment with folic acid improves nitric oxide bioavailability and decreases superoxide production in human vessels, through tetrahydrobiopterin-mediated improvement of eNOS coupling
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Intravenous infusion of 5-methyl-tetrahydrofolate rapidly improves eNOS Coupling. In human vessels by increasing tetrahydrobiopterin bioavailability
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5-Methyl-tetrahydrofolate acid improves endothelial function and decreases superoxide production by improving eNOS coupling and increasing tetrahydrobiopterin bioavailability in human vessels in vivo
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A Novel Haplotype on GCH1 Gene, Encoding GTP Cyclohydrolase 1, Regulates Vascular Biopterin Synthesis, eNOS Coupling and Vascular Redox in Human Vessels
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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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Plasma asymmetrical-dimethyl-arginine (ADMA) regulates nitric oxide bioavailability and vascular superoxide production in human vessels
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Plasma levels of sCD40-ligand interact with homocysteine biosynthetic pathway and predict eNOS coupling in human vessels: effects on vascular redox state
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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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Soluble CD40-ligand levels are associated with vascular superoxide production and eNOS coupling in human vessels: Interrelationships with homocysteine biosynthetic pathway
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5-methyl-tetrahydrofolate increases eNOS activity by preventing peroxynitrite-induced oxidation of tetrahydrobiopterin in human vessels
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Association of plasma asymmetrical dimethylarginine (ADMA) with elevated vascular superoxide production and endothelial nitric oxide synthase uncoupling: implications for endothelial function in human atherosclerosis.
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Low- and high- dose treatment with folic acid, equally improve endothelial function and decrease superoxide production in human vessels via tetrahydrobiopterin-mediated eNOS coupling
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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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5-Methyl-tetrahydrofolic acid rapidly improves endothelial function and superoxide production in human atherosclerosis: Effects on tetrahyd robiopterin-dependent eNOS coupling
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Altered plasma vs. vascular biopterins in human atherosclerosis reveal relationships between endothelial nitric oxide synthase coupling, endothelial function and inflammation
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The gene polymorphisms of eNOS and MTHFR modulates the development of preeclampsia in Han population
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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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Vascular Homocysteine Versus 5-Methyl-Tetrahydrofolate As Regulators of Vascular Redox and Endothelial Function in Human Vessels
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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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Relationships between vascular/plasma biopterins and endothelial nitric oxide synthase coupling, endothelial function and inflammation, in human atherosclerosis
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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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Genetic polymorphisms G894T on the eNOS gene is associated with endothelial function and vWF levels in premature myocardial infarction survivors.
by: Antoniades, C, et al.
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Altered plasma versus vascular biopterins in human atherosclerosis reveal relationships between endothelial nitric oxide synthase coupling, endothelial function, and inflammation.
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Redox state in arterial grafts predicts left ventricular functional restoration after coronary artery bypass grafting
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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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Preoperative evaluation of flow-mediated dilatation in the left radial artery or the right brachial artery, as a predictor of nitric-oxide bioavailability in coronary artery bypass grafts
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Vascular Homocysteine vs 5-Methyl-Tetrahydrofolate as Regulators of Vascular Redox and Endothelial Function in Human Vessels
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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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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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Polymorphism of MTHFR gene affects vascular redox and nitric oxide bioavailability by modifying eNOS coupling

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