Cellular and Molecular Basis of Wound Healing in Diabetes.
From: Wound Healing and Vascular Biology Laboratory, Division of Plastic Surgery, Columbia University College of Physicians and Surgeons, 5141 Broadway, New York, NY 10034, USA. hb2133@columbia.edu
The Journal of clinical investigation
- Publish Date: May 2007
- ISSN: 0021-9738
- Volume: 117
- Issue: 5
- Pages: 1219-22
- Medium: Print
- Language: English
- Citation (JAMA): Brem Harold, Tomic-Canic Marjana, et al. Cellular and Molecular Basis of Wound Healing in Diabetes.. J. Clin. Invest. May 2007;117:1219-22
Abstract
Diabetic foot ulcers (DFUs), a leading cause of amputations, affect 15% of people with diabetes. A series of multiple mechanisms, including decreased cell and growth factor response, lead to diminished peripheral blood flow and decreased local angiogenesis, all of which can contribute to lack of healing in persons with DFUs. In this issue of the JCI, Gallagher and colleagues demonstrate that in diabetic mice, hyperoxia enhances the mobilization of circulating endothelial progenitor cells (EPCs) from the bone marrow to the peripheral circulation (see the related article beginning on page 1249). Local injection of the chemokine stromal cell-derived factor-1alpha then recruits these EPCs to the cutaneous wound site, resulting in accelerated wound healing. Thus, Gallagher et al. have identified novel potential targets for therapeutic intervention in diabetic wound healing.
Mesh Headings (Keywords): Animals, Diabetic Foot, Humans, Wound Healing
Check for Full Text / PubMed Unique Identifier (PMID): 17476353
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