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Abstract
The normal healing of a cutaneous wound is achieved via well-orchestrated integration of complex biological and molecular events of cell migration, proliferation, extracellular matrix deposition and tissue remodeling. Chronic wounds fail to progress through the normal stages of healing, and enter a state of pathologic inflammation. Complicated diabetic patients show delayed wound healing caused by multiple factors including vascular insufficiency, abnormalities of the biochemical environment and hyperglycemia per se. Novel technologies including growth factor therapy, gene therapy, stem cell technologies, synthetic skins and hyperbaric oxygen treatment are under development. In the near future, these therapeutic strategies will be clinically available.
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Fig. 2
Minicircle-VEGF165 gene delivery via sonoporation enhanced wound closure and increased blood perfusion in the wound tissue of treated diabetic mice. A. Macroscopic pictures of the wounds. B. Average area (in pixels) of the wounds of the minicircle-VEGF165 treated diabetic mice was significantly small as compared with those of diabetic control and pβ-VEGF165 treated diabetic mice. Minicircle-VEGF165 treatment promoted diabetic wound closure (*P < 0.05). (adapted form reference 58).
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