Tetrahydrobiopterin: coupling nitric oxide and redox signalling in cardiovascular disease

Tetrahydrobiopterin: coupling nitric oxide and redox signalling in cardiovascular disease

Chi tiết về thư mục
Tác giả chính:	Channon, K
Định dạng:	Conference item
Được phát hành:	2012

Những quyển sách tương tự

Tetrahydrobiopterin: regulator of endothelial nitric oxide synthase in vascular disease.
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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
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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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Regulation of endothelial nitric oxide synthase (eNOS) by tetrahydrobiopterin in vascular disease
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Free radicals and redox signalling in cardiovascular disease: introduction
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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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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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Redox sensor and effector functions of tetrahydrobiopterin and the mitochondria in molecular models of cardiovascular disease
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Tetrahydrobiopterin: pleiotropic roles in cardiovascular pathophysiology.
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Endothelial tetrahydrobiopterin deficiency accelerates atherosclerotic progression by nitric oxide synthase uncoupling
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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 nitric oxide synthase dysfunction in diabetic mice: importance of tetrahydrobiopterin in eNOS 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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Reduced levels of tetrahydrobiopterin in diabetic mouse model: Effects on endothelial function and nitric oxide (NO) synthase dimerisation
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Polymorphism of MTHFR gene affects vascular redox and nitric oxide bioavailability by modifying eNOS coupling
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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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Nitric oxide Bioavailability is preserved in diabetes by increased endothelial tetrahydrobiopterin synthesis in targeted GTP cyclohydrolase transgenic mice
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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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Genetic variability of MTHFR affects vascular redox and nitric oxide bioavailability in human vessels, by modifying eNOS coupling
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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.
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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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