Validating the GTP-cyclohydrolase 1-feedback regulatory complex as a therapeutic target using biophysical and in vivo approaches.

Validating the GTP-cyclohydrolase 1-feedback regulatory complex as a therapeutic target using biophysical and in vivo approaches.

BACKGROUND AND PURPOSE: 6R-L-erythro-5,6,7,8-tetrahydrobiopterin (BH4 ) is an essential cofactor for nitric oxide biosynthesis. Substantial clinical evidence indicates that intravenous BH4 restores vascular function in patients. Unfortunately, oral BH4 has limited efficacy. Therefore, orally bioavai...

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Manylion Llyfryddiaeth
Prif Awduron:	Hussein, D, Starr, A, Heikal, L, McNeill, E, Channon, K, Brown, P, Sutton, B, McDonnell, J, Nandi, M
Fformat:	Journal article
Iaith:	English
Cyhoeddwyd:	Wiley 2015

Eitemau Tebyg

Overexpression of GTP cyclohydrolase 1 feedback regulatory protein is protective in a murine model of septic shock.
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GTP cyclohydrolase I expression, protein, and activity determine intracellular tetrahydrobiopterin levels, independent of GTP cyclohydrolase feedback regulatory protein expression.
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Cell-autonomous role of endothelial GTP cyclohydrolase 1 and tetrahydrobiopterin in blood pressure regulation
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GTP Cyclohydrolase 1/Tetrahydrobiopterin Counteract Ferroptosis through Lipid Remodeling
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Cardiomyocyte GTP cyclohydrolase 1 and tetrahydrobiopterin increase NOS1 activity and accelerate myocardial relaxation
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Cardiomyocyte-targeted overexpression of GTP cyclohydrolase-1 increases nNOS activity and hastens myocardial relaxation
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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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Endothelium-targeted GTP cyclohydrolase I overexpression inhibits wire injury-induced restenosis in mouse carotid artery
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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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Endothelium-specific GTP cyclohydrolase I overexpression attenuates blood pressure progression in salt-sensitive low-renin hypertension.
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