Endothelium-specific GTP cyclohydrolase I overexpression accelerates refractory wound healing by suppressing oxidative stress in diabetes.
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The protein partners of GTP cyclohydrolase I in rat organsManganese superoxide dismutase expression in endothelial progenitor cells accelerates wound healing in diabetic mice.Nox2-dependent glutathionylation of endothelial NOS leads to uncoupled superoxide production and endothelial barrier dysfunction in acute lung injury.AMP-activated protein kinase rescues the angiogenic functions of endothelial progenitor cells via manganese superoxide dismutase induction in type 1 diabetes.Angiogenesis in diabetes and obesityDipyridamole reverses peripheral ischemia and induces angiogenesis in the Db/Db diabetic mouse hind-limb model by decreasing oxidative stress.Akt/hypoxia-inducible factor-1α signaling deficiency compromises skin wound healing in a type 1 diabetes mouse modelEndothelial dysfunction and diabetes: effects on angiogenesis, vascular remodeling, and wound healing.Sirtuin-6 deficiency exacerbates diabetes-induced impairment of wound healing.Thrombospondin-1/CD36 pathway contributes to bone marrow-derived angiogenic cell dysfunction in type 1 diabetes via Sonic hedgehog pathway suppression.Multiple therapeutic effect of endothelial progenitor cell regulated by drugs in diabetes and diabetes related disorder.Protein Phosphotyrosine Phosphatase 1B (PTP1B) in Calpain-dependent Feedback Regulation of Vascular Endothelial Growth Factor Receptor (VEGFR2) in Endothelial Cells: IMPLICATIONS IN VEGF-DEPENDENT ANGIOGENESIS AND DIABETIC WOUND HEALING.Is There a Role for Bioactive Lipids in the Pathobiology of Diabetes Mellitus?Advanced glycation end products delay corneal epithelial wound healing through reactive oxygen species generation.Bee Venom Accelerates Wound Healing in Diabetic Mice by Suppressing Activating Transcription Factor-3 (ATF-3) and Inducible Nitric Oxide Synthase (iNOS)-Mediated Oxidative Stress and Recruiting Bone Marrow-Derived Endothelial Progenitor Cells.Folic acid may be a potential addition to diabetic foot ulcer treatment - a hypothesis.Deficiency of endothelial nitric oxide signaling pathway exacerbates peritoneal fibrosis in mice.Transplantation of cyclic stretched fibroblasts accelerates the wound-healing process in streptozotocin-induced diabetic mice.
P2860
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P2860
Endothelium-specific GTP cyclohydrolase I overexpression accelerates refractory wound healing by suppressing oxidative stress in diabetes.
description
article científic
@ca
article scientifique
@fr
articolo scientifico
@it
artigo científico
@pt
bilimsel makale
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scientific article published on 31 March 2009
@en
vedecký článok
@sk
vetenskaplig artikel
@sv
videnskabelig artikel
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vědecký článek
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name
Endothelium-specific GTP cyclo ...... oxidative stress in diabetes.
@en
Endothelium-specific GTP cyclo ...... oxidative stress in diabetes.
@nl
type
label
Endothelium-specific GTP cyclo ...... oxidative stress in diabetes.
@en
Endothelium-specific GTP cyclo ...... oxidative stress in diabetes.
@nl
prefLabel
Endothelium-specific GTP cyclo ...... oxidative stress in diabetes.
@en
Endothelium-specific GTP cyclo ...... oxidative stress in diabetes.
@nl
P2093
P2860
P1476
Endothelium-specific GTP cyclo ...... oxidative stress in diabetes.
@en
P2093
P2860
P304
P356
10.1152/AJPENDO.00150.2009
P577
2009-03-31T00:00:00Z