Advanced glycation end-products (AGE) are complex compounds linked to diabetes-related complications. Their role as a cause or consequence of these complications is unclear. This review discusses AGE formation, their patho-biochemistry, and their role in diabetic microvascular complications like retinopathy, neuropathy, and nephropathy. Carbonyl stress is proposed as a cause of AGE toxicity. AGE concentrations vary with age, diabetes, and its complications. Current methods for detecting and measuring AGE lack universal standards, making comparisons difficult. Aminoguanidine, a drug that cleaves AGE-induced cross-links, has shown promise in reducing diabetes-related complications in clinical trials. AGE form through non-enzymatic reactions between reducing sugars and amino groups in proteins, lipids, and nucleic acids. This process, known as the Maillard reaction, produces Schiff bases and Amadori products, leading to AGE. AGE formation is influenced by factors like glucose concentration, transitional metals, and oxidative stress. AGE include compounds like CML, pentosidine, and pyralline, which are associated with oxidative stress and vascular damage. AGE accumulation is linked to various diseases, including diabetes, rheumatoid arthritis, and end-stage renal disease. AGE are involved in vascular damage, including atherosclerosis and accelerated vascular damage in diabetes. They interact with AGE receptors like RAGE, leading to oxidative stress, inflammation, and vascular dysfunction. AGE-RAGE interactions activate NF-κB, contributing to endothelial dysfunction and vascular disease. AGE also affect coagulation and fibrinolysis, promoting a procoagulant state. AGE concentrations increase in diabetes, with higher levels in diabetic patients compared to controls. AGE accumulation is associated with diabetic complications like retinopathy, neuropathy, and nephropathy. AGE are found in various tissues, including the lens, kidney, and vascular system. AGE levels rise with age and are higher in diabetic patients. AGE are measured using methods like HPLC, ELISA, and immunohistochemistry, but there is no universally accepted standard. AGE formation is linked to vascular dysfunction, including endothelial dysfunction, oxidative stress, and vascular thickening. AGE contribute to diabetic retinopathy by increasing retinal endothelial cell permeability and inducing growth factors like VEGF. AGE are also involved in cataract formation by glycation of lens crystallin and the Na+/K+-ATPase pump. Diabetic neuropathy is associated with AGE accumulation in the vasa nervorum, leading to wall thickening, ischaemia, and myelin damage. AGE accumulation in the kidney is linked to diabetic nephropathy, with increased extracellular matrix expansion and glomerular sclerosis. TGF-β, a prosclerotic cytokine, is involved in the pathogenesis of diabetic nephropathy. AGE inhibitors like OPB 9195 have shown promise in reducing diabetic nephropathy progression. AGE are also involved inAdvanced glycation end-products (AGE) are complex compounds linked to diabetes-related complications. Their role as a cause or consequence of these complications is unclear. This review discusses AGE formation, their patho-biochemistry, and their role in diabetic microvascular complications like retinopathy, neuropathy, and nephropathy. Carbonyl stress is proposed as a cause of AGE toxicity. AGE concentrations vary with age, diabetes, and its complications. Current methods for detecting and measuring AGE lack universal standards, making comparisons difficult. Aminoguanidine, a drug that cleaves AGE-induced cross-links, has shown promise in reducing diabetes-related complications in clinical trials. AGE form through non-enzymatic reactions between reducing sugars and amino groups in proteins, lipids, and nucleic acids. This process, known as the Maillard reaction, produces Schiff bases and Amadori products, leading to AGE. AGE formation is influenced by factors like glucose concentration, transitional metals, and oxidative stress. AGE include compounds like CML, pentosidine, and pyralline, which are associated with oxidative stress and vascular damage. AGE accumulation is linked to various diseases, including diabetes, rheumatoid arthritis, and end-stage renal disease. AGE are involved in vascular damage, including atherosclerosis and accelerated vascular damage in diabetes. They interact with AGE receptors like RAGE, leading to oxidative stress, inflammation, and vascular dysfunction. AGE-RAGE interactions activate NF-κB, contributing to endothelial dysfunction and vascular disease. AGE also affect coagulation and fibrinolysis, promoting a procoagulant state. AGE concentrations increase in diabetes, with higher levels in diabetic patients compared to controls. AGE accumulation is associated with diabetic complications like retinopathy, neuropathy, and nephropathy. AGE are found in various tissues, including the lens, kidney, and vascular system. AGE levels rise with age and are higher in diabetic patients. AGE are measured using methods like HPLC, ELISA, and immunohistochemistry, but there is no universally accepted standard. AGE formation is linked to vascular dysfunction, including endothelial dysfunction, oxidative stress, and vascular thickening. AGE contribute to diabetic retinopathy by increasing retinal endothelial cell permeability and inducing growth factors like VEGF. AGE are also involved in cataract formation by glycation of lens crystallin and the Na+/K+-ATPase pump. Diabetic neuropathy is associated with AGE accumulation in the vasa nervorum, leading to wall thickening, ischaemia, and myelin damage. AGE accumulation in the kidney is linked to diabetic nephropathy, with increased extracellular matrix expansion and glomerular sclerosis. TGF-β, a prosclerotic cytokine, is involved in the pathogenesis of diabetic nephropathy. AGE inhibitors like OPB 9195 have shown promise in reducing diabetic nephropathy progression. AGE are also involved in