Tetrahydrobiopterin-dependent preservation of nitric oxide-mediated endothelial function in diabetes by targeted transgenic GTP-cyclohydrolase I overexpression.
Increased production of reactive oxygen species and loss of endothelial NO bioactivity are key features of vascular disease states such as diabetes mellitus. Tetrahydrobiopterin (BH4) is a required cofactor for eNOS activity; pharmacologic studies suggest that BH4 may mediate some of the adverse eff...
Egile Nagusiak: | Alp, N, Mussa, S, Khoo, J, Cai, S, Guzik, T, Jefferson, A, Goh, N, Rockett, K, Channon, K |
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Formatua: | Journal article |
Hizkuntza: | English |
Argitaratua: |
2003
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Antzeko izenburuak
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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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Tetrahydrobiopterin-dependent preservation of nitric oxide-mediated endothelial function in diabetes by targeted transgenic GTP-cyclohydrolase I over-expression
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Endothelial-targeted GTP cyclohydrolase I overexpression increases endothelial tetrahydrobiopterin levels and preserves eNOS coupling in eNOS overexpressing mice
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Increased endothelial tetrahydrobiopterin synthesis by targeted transgenic GTP-cyclohydrolase I overexpression reduces endothelial dysfunction and atherosclerosis in ApoE-knockout mice.
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Nitric oxide bioactivity in ApoE -/- mice is maintained by increased endothelial tetrahydrobiopterin synthesis via targeted GTP cyclohydrolase-1 over-expression
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