Advanced glycation end-products (AGEs) are a complex group of compounds implicated in diabetes-related complications, though their role as causes or consequences remains unclear. This review discusses the chemistry of AGE formation, their patho-biochemistry, particularly in diabetic microvascular complications such as retinopathy, neuropathy, and nephropathy, and their role in accelerated vasculopathy. The concept of carbonyl stress, which involves the accumulation of reactive carbonyls, is highlighted. The review also addresses the challenges in detecting and measuring AGEs, including the lack of a universally accepted method or unit of measurement. Recent phase III trials using aminoguanidine, a drug that cleaves AGE-induced chemical cross-links, show promise in limiting the progression of diabetes-related complications. The formation and structure of AGEs, their interaction with AGE receptors, and their consequences at the tissue level are discussed, along with their metabolism and concentrations in diabetes, chronological age, and renal failure. The review concludes by examining the effects of AGEs on diabetic retinopathy, cataract formation, neuropathy, and nephropathy, as well as their role in diabetic atherosclerotic disease.Advanced glycation end-products (AGEs) are a complex group of compounds implicated in diabetes-related complications, though their role as causes or consequences remains unclear. This review discusses the chemistry of AGE formation, their patho-biochemistry, particularly in diabetic microvascular complications such as retinopathy, neuropathy, and nephropathy, and their role in accelerated vasculopathy. The concept of carbonyl stress, which involves the accumulation of reactive carbonyls, is highlighted. The review also addresses the challenges in detecting and measuring AGEs, including the lack of a universally accepted method or unit of measurement. Recent phase III trials using aminoguanidine, a drug that cleaves AGE-induced chemical cross-links, show promise in limiting the progression of diabetes-related complications. The formation and structure of AGEs, their interaction with AGE receptors, and their consequences at the tissue level are discussed, along with their metabolism and concentrations in diabetes, chronological age, and renal failure. The review concludes by examining the effects of AGEs on diabetic retinopathy, cataract formation, neuropathy, and nephropathy, as well as their role in diabetic atherosclerotic disease.