(From ScienceDaily). Diabetes is often used as a model for aging by researchers, as some of the underlying mechanisms or consequences are similar. Here, researches examine the mechanisms by which healing works, and then ceases to work with disease progression. " Endothelial progenitor cells (EPCs), which derive from bone marrow, normally travel to sites of injury and are essential for the formation of blood vessels and wound healing. ... The authors examined diabetic mice and found that increased oxygen levels (hyperoxia) enhanced the mobilization of EPCs from the bone marrow to the peripheral blood circulation. The high oxygen levels increased the activation of the bone marrow enzyme eNOS, which stimulated nitric oxide production, helping to produce greater numbers of EPCs. However, local injection of the chemokine stromal cell-derived factor 1 alpha (SDF-1alpha) was required to recruit these EPCs from the circulation to the wound site. The increased presence of EPCs at the wound site resulted in accelerated wound healing. The authors concluded that impaired eNOS activation and decreased SDF-1alpha expression in diabetes are responsible for the defect in diabetic wound healing." Failures in this healing process exist in aging due to the accumulation of damage in vital components of our biochemistry. We should hurry to repair that damage just as we hurry to cure diabetes.