Diabetic impairments in NO-mediated endothelial progenitor cell mobilization and homing are reversed by hyperoxia and SDF-1 alpha.
By Katherine A. Gallagher, Zhao-Jun Liu, M. Xiao, Haiying Chen, L. Goldstein, D. Buerk, April E. Nedeau, S. Thom, O. Velazquez. Journal of Clinical Investigation, 2007
674 citations recorded by the source corpus.
Subfields: Cell Biology, Molecular Biology, Oncology
View Paper: https://www.semanticscholar.org/paper/b1ac9de575bdb519f09b3660be8fb411785be3b3
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Citations in the corpus
- Acute and Impaired Wound Healing: Pathophysiology and Current Methods for Drug Delivery, Part 1: Normal and Chronic Wounds: Biology, Causes, and Approaches to Care (2012, background): “In fact, key signaling intermediates responsible for coordinating/regulating wound healing angiogenesis and vasculogenesis may be dysfunctional during diabetes.(14) Indeed, diabetic patients prone to the development of chronic wounds(11) may exhibit deficiencies in either EPC bone marrow release or ”
- Factors affecting wound healing (2010, background): “…restoration of vasculature in diabetic wounds have implied that EPC mobilization and homing are impaired, and that the level of VEGF, the primary proangiogenic factor in wounds, is decreased in the diabetic state (Brem and Tomic-Canic, 2007; Gallagher et al., 2007; Quattrini et al., 2008).”
- Recent advances on the development of wound dressings for diabetic foot ulcer treatment--a review. (2013, background): “SDF-1a STZ diabetic mice Increased EPC mobilization, homing and wound healing Gallagher et al, 2007 [260]”
- Endothelial Dysfunction and Diabetes: Effects on Angiogenesis, Vascular Remodeling, and Wound Healing (2012, background): “Bone-marrow-derived EPCs are mobilized to wound sites by eNOS activation in the bone marrow which is impaired in diabetics [257].”