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Endothelium-specific GTP cyclohydrolase I overexpression accelerates refractory wound healing by suppressing oxidative stress in diabetes.

Abstract:

Refractory wound is a severe complication that leads to limb amputation in diabetes. Endothelial nitric oxide synthase (eNOS) plays a key role in normal wound repair but is uncoupled in streptozotocin (STZ)-induced type 1 diabetes because of reduced cofactor tetrahydrobiopterin (BH(4)). We tested the hypothesis that overexpression of GTP cyclohydrolase I (GTPCH I), the rate-limiting enzyme for de novo BH(4) synthesis, retards NOS uncoupling and accelerates wound healing in STZ mice. Blood glu...

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Publication status:
Published

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Publisher copy:
10.1152/ajpendo.00150.2009

Authors


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Institution:
University of Oxford
Department:
Oxford, MSD, RDM, Cardiovascular Medicine, BHF Centre of Research Excellence
Role:
Author
Journal:
American journal of physiology. Endocrinology and metabolism
Volume:
296
Issue:
6
Pages:
E1423-E1429
Publication date:
2009-06-05
DOI:
EISSN:
1522-1555
ISSN:
0193-1849
URN:
uuid:8e16bca2-925c-4837-8901-fcca37d321b0
Source identifiers:
4369
Local pid:
pubs:4369

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