Tetrahydrobiopterin: coupling nitric oxide and redox signalling in cardiovascular disease

Tetrahydrobiopterin: coupling nitric oxide and redox signalling in cardiovascular disease

מידע ביבליוגרפי
מחבר ראשי:	Channon, K
פורמט:	Conference item
יצא לאור:	2012

פריטים דומים

Tetrahydrobiopterin and nitric oxide synthase recouplers
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Tetrahydrobiopterin: regulator of endothelial nitric oxide synthase in vascular disease.
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Regulation of endothelial nitric oxide synthase by tetrahydrobiopterin in vascular disease.
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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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Tetrahydrobiopterin protects against hypertrophic heart disease independent of myocardial nitric oxide synthase coupling.
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Tetrahydrobiopterin protects against hypertrophic heart disease independent of myocardial nitric oxide synthase coupling
מאת: Hashimoto, T, et al.
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Regulation of endothelial nitric oxide synthase (eNOS) by tetrahydrobiopterin in vascular disease
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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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The role of tetrahydrobiopterin in inflammation and cardiovascular disease.
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Tetrahydrobiopterin deficiency uncouples nitric oxide synthase and causes pulmonary hypertension
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Dihydrofolate reductase protects endothelial nitric oxide synthase from uncoupling in tetrahydrobiopterin deficiency.
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Dihydrofolate reductase protects endothelial nitric oxide synthase from uncoupling in tetrahydrobiopterin deficiency
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Endothelial tetrahydrobiopterin deficiency accelerates atherosclerotic progression by nitric oxide synthase uncoupling
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Tetrahydrobiopterin Prevents Lung Ischemia/reperfusion-Induced Uncoupling of Endothelial Nitric Oxide Synthase
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Tetrahydrobiopterin: pleiotropic roles in cardiovascular pathophysiology.
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Endothelial nitric oxide synthase dysfunction in diabetic mice: importance of tetrahydrobiopterin in eNOS dimerisation.
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Redox sensor and effector functions of tetrahydrobiopterin and the mitochondria in molecular models of cardiovascular disease
מאת: Bailey, J
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Free radicals and redox signalling in cardiovascular disease: introduction
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Reduced levels of tetrahydrobiopterin in diabetic mouse model: Effects on endothelial function and nitric oxide (NO) synthase dimerisation
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Recoupling the cardiac nitric oxide synthases: tetrahydrobiopterin synthesis and recycling.
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Recoupling the cardiac nitric oxide synthases: Tetrahydrobiopterin synthesis and recycling
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Nitric oxide Bioavailability is preserved in diabetes by increased endothelial tetrahydrobiopterin synthesis in targeted GTP cyclohydrolase transgenic mice
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Quantitative regulation of intracellular endothelial nitric-oxide synthase (eNOS) coupling by both tetrahydrobiopterin-eNOS stoichiometry and biopterin redox status: insights from cells with tet-regulated GTP cyclohydrolase I expression.
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A Novel Role for Endothelial Tetrahydrobiopterin in Mitochondrial Redox Balance
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Critical role for tetrahydrobiopterin recycling by dihydrofolate reductase in regulation of endothelial nitric-oxide synthase coupling: relative importance of the de novo biopterin synthesis versus salvage pathways.
מאת: Crabtree, M, et al.
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Prevention of hypoxia-induced pulmonary hypertension and vascular remodelling by targeting endothelial tetrahydrobiopterin-dependent nitric oxide synthase regulation
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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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Polymorphism of MTHFR gene affects vascular redox and nitric oxide bioavailability by modifying eNOS coupling
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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
מאת: Antoniades, C, et al.
יצא לאור: (2007)

P683The role of nitric oxide synthase (NOS) and its essential cofactor tetrahydrobiopterin (BH4) in diabetic cardiomyopathy.
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Tetrahydrobiopterin-dependent preservation of nitric oxide-mediated endothelial function in diabetes by targeted transgenic GTP-cyclohydrolase I overexpression.
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GFRP tonically inhibits production of tetrahydrobiopterin and nitric oxide in marine endothelial cells
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Adenovirus-mediated GTP cyclohydrolase I gene delivery augments tetrahydrobiopterin and restores nitric oxide synthase function in hyperglycaemic human aortic endothelial cells
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