Impaired wound healing is an important diabetic complication associated with increased morbidity and mortality. It appears to be the net result of micro‐ and macrovascular disease. Diabetic neuropathy and the resulting loss of protective sensation (LOPS) has been recognized as one of the major causes for delayed healing in diabetic foot ulcer patients. In addition, hyperglycemia and a number of hyperglycemia‐related factors have been linked to impaired diabetic wound healing, including advanced glycation end products (AGE). A large body of evidence from in vitro and in vivo studies and also data from studies using anti‐AGE agents, indicate that AGE may play a role in the pathogenesis of impaired diabetic wound healing. AGE affect the wound healing process either directly by their interference with a variety of components involved or indirectly through their association with diabetic neuropathy and/or angiopathy. However, further studies need to be performed, mostly clinical studies, to evaluate the exact role of AGE in the impaired diabetic wound healing, suggesting new therapeutic approaches.