Division of Cardiovascular Medicine, Diabetes and Obesity Center, University of Louisville School of Medicine, Louisville, Kentucky 40202, USA.
Curr Opin Endocrinol Diabetes Obes. 2012 Apr;19(2):104-8. doi: 10.1097/MED.0b013e3283514e00.
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.
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.
Stimulating resolution with proresolving lipid mediators may represent a novel strategy for promoting wound healing in diabetes.
1 型和 2 型糖尿病最显著的临床表现之一是伤口愈合不良。随着全球糖尿病发病率的上升，迫切需要详细了解导致糖尿病患者炎症持续存在和伤口愈合延迟的分子和细胞缺陷。新出现的证据表明，炎症的及时消退部分是由内源性的促解决脂质介质（如 resolvins）介导的。在这里，我们回顾了在解决和糖尿病领域的最新进展，并强调了新型促解决策略在促进糖尿病伤口愈合方面的潜力。
糖尿病患者伤口愈合不良的一个关键潜在特征是巨噬细胞功能障碍。这与凋亡细胞清除缺陷、感染风险增加和血管生成改变有关。糖尿病和肥胖与慢性炎症和生物活性脂质介质生物合成改变有关，这些改变促进炎症的消退。用促解决脂质介质刺激解决可改善糖尿病患者的代谢参数，减弱全身炎症，恢复受损的巨噬细胞吞噬作用，并加速肥胖和糖尿病动物模型的伤口愈合。
用促解决脂质介质刺激解决可能代表促进糖尿病伤口愈合的一种新策略。
