Abstract
Impaired diabetic wound healing (WH) constitutes a serious diabetic complication with increased morbidity, mortality and health expenditure. The exact pathogenetic mechanisms have not been fully clarified. A variety of hyperglycemia and oxidative stress related factors, have been proposed, including advanced glycaction end products (AGE). The existing literature data, support the role of AGE in the pathogenesis of diabetic complications, namely micro- and macro- angiopathy which underlie delayed diabetic WH. In addition, a large body of evidence support a direct negative effect of AGE in the WH process by their interference with various components involved in the cascade following skin injury. Endogenously formed or exogenously derived AGE, in a similar manner, affect negatively the WH process in diabetes. It is obvious that further studies are needed to clarify the exact role of AGE in the impaired diabetic WH and offer possible new therapeutic strategies
Keywords: Advanced glycation end products, AGE, Ncarboxymethyllysine (CML), Methylglyoxal (MG), Diabetic wound healing, Oxidative stress, Inflammation, LDL, Diabetic Nephropathy, Diabetic Retinopathy
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