title: Proresolving lipid mediators and diabetic wound healing.
abstract: OBJECTIVE
  Defective wound healing is one of the most prominent clinical manifestations of both type 1 and type 2 diabetes. As the global rates of diabetes increase, a detailed understanding of the molecular and cellular defects that give rise to unresolved inflammation and delayed wound healing in diabetes is urgently required. Emerging evidence indicates that timely resolution of inflammation is mediated in part by endogenous proresolving lipid mediators, such as resolvins. Here, we review recent advances in the area of resolution and diabetes and highlight the potential of novel proresolving strategies for promoting wound healing in diabetes.
  
  
  RESULTS
  Macrophage dysfunction is a critical underlying feature of altered wound healing in diabetic patients. This is associated with defective clearance of apoptotic cells, increased risk of infection, and altered angiogenesis. Diabetes and obesity are associated with chronic inflammation and altered biosynthesis of bioactive lipid mediators that promote the resolution of inflammation. Stimulating resolution with proresolving lipid mediators improves metabolic parameters in diabetes, blunts systemic inflammation, restores defective macrophage phagocytosis, and accelerates wound healing in animal models of obesity and diabetes.
  
  
  CONCLUSIONS
  Stimulating resolution with proresolving lipid mediators may represent a novel strategy for promoting wound healing in diabetes.
authors.affiliation: Division of Cardiovascular Medicine, Diabetes and Obesity Center, University of Louisville School of Medicine, Louisville, Kentucky 40202, USA.
authors.forename: Jason
authors.initials: J
authors.lastname: Hellmann
authors.forename: Yunan
authors.initials: Y
authors.lastname: Tang
authors.forename: Matthew
authors.initials: M
authors.lastname: Spite
mesh_terms: D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D003922:Diabetes Mellitus, Type 1 / Q000150:complications / Q000188:drug therapy* / Q000378:metabolism; D003924:Diabetes Mellitus, Type 2 / Q000150:complications / Q000188:drug therapy* / Q000378:metabolism; D015777:Eicosanoids / Q000096:biosynthesis / Q000494:pharmacology; D005260:Female; D006801:Humans; D007249:Inflammation / Q000188:drug therapy* / Q000378:metabolism; D015289:Leukotrienes / Q000096:biosynthesis / Q000494:pharmacology; D008264:Macrophages / Q000187:drug effects; D008297:Male; D011453:Prostaglandins / Q000096:biosynthesis / Q000494:pharmacology; D014456:Ulcer / Q000188:drug therapy* / Q000209:etiology; D014945:Wound Healing / Q000187:drug effects*
chemical_list: D000893:Anti-Inflammatory Agents; D015777:Eicosanoids; D015289:Leukotrienes; D011453:Prostaglandins