title: Cellular and molecular basis of wound healing in diabetes.
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.
authors.affiliation: 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
authors.forename: Harold
authors.initials: H
authors.lastname: Brem
authors.forename: Marjana
authors.initials: M
authors.lastname: Tomic-Canic
mesh_terms: D000818:Animals; D017719:Diabetic Foot / Q000378:metabolism* / Q000473:pathology* / Q000503:physiopathology; D006801:Humans; D014945:Wound Healing / Q000502:physiology*