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Shafi Mussa

Researcher at John Radcliffe Hospital

Publications -  18
Citations -  2225

Shafi Mussa is an academic researcher from John Radcliffe Hospital. The author has contributed to research in topics: Radial artery & Tetrahydrobiopterin. The author has an hindex of 12, co-authored 17 publications receiving 2163 citations. Previous affiliations of Shafi Mussa include University of Oxford.

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Mechanisms of Increased Vascular Superoxide Production in Human Diabetes Mellitus Role of NAD(P)H Oxidase and Endothelial Nitric Oxide Synthase

TL;DR: These observations suggest important roles for NAD(P)H oxidases, endothelial NO synthase uncoupling, and protein kinase C signaling in mediating increased vascular superoxide production and endothelial dysfunction in human diabetes mellitus.
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Tetrahydrobiopterin-dependent preservation of nitric oxide–mediated endothelial function in diabetes by targeted transgenic GTP–cyclohydrolase I overexpression

TL;DR: In this article, the authors investigated the importance and mechanisms of Tetrahydrobiopterin availability in vivo using a novel transgenic mouse model with endothelial-targeted overexpression of the rate-limiting enzyme in BH4 synthesis, guanosine triphosphate-cyclohydrolase I (GTPCH).
Journal Article

Tetrahydrobiopterin-dependent preservation of nitric oxide-mediated endothelial function in diabetes by targeted transgenic GTP-cyclohydrolase I over-expression

TL;DR: Findings indicate that BH4 is an important mediator of eNOS regulation in diabetes and is a rational therapeutic target to restore NO-mediated endothelium-dependent vasodilatation in Diabetes and other vascular disease states.
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Endothelial nitric oxide synthase dysfunction in diabetic mice: importance of tetrahydrobiopterin in eNOS dimerisation.

TL;DR: The results demonstrate that BH4 plays an important role in regulating eNOS activity and its functional protein structure, suggesting that increasing endothelial BH 4 and/or protecting it from oxidation may be a rational therapeutic strategy to restore eN OS function in diabetes.