- 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...
Expand abstract - Publication status:
- Published
- Publisher copy:
- 10.1152/ajpendo.00150.2009
-
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- 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
- Copyright date:
- 2009
Journal article
Endothelium-specific GTP cyclohydrolase I overexpression accelerates refractory wound healing by suppressing oxidative stress in diabetes.
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