Role of Advanced Glycation End Products, Oxidative Stress, and Inflammation in Diabetic Vascular Complications

Diabetic vascular complication is a leading cause of end-stage renal failure, acquired blindness, a variety of neuropathies, and accelerated atherosclerosis. Recent large prospective clinical studies have shown that intensive glucose control effectively reduces microvascular complications among patients with diabetes. It is now well established that formation and accumulation of advanced glycation end products (AGEs) progress during normal aging, and at an extremely accelerated rate under diabetes, thus being implicated in diabetic vascular complications. Moreover, there is accumulating evidence that AGE and the receptor for AGE (RAGE) interaction elicits oxidative stress generation and subsequently evokes inflammation in vascular wall cells. In addition, digested food-derived AGEs play an important role in the pathogenesis of diabetic vascular complications. These observations suggest that the AGE-RAGE axis and other hyperglycemia-related metabolic derangements are interrelated to each other, being involved in diabetic vascular complications. This chapter discusses the role of AGEs in diabetic retinopathy, diabetic nephropathy, and cardiovascular diseases.