Advanced glycation end products (AGEs) are formed through non-enzymatic glycation of proteins in diabetes, contributing to various complications such as retinopathy, nephropathy, neuropathy, and cardiomyopathy. AGEs form cross-links with proteins, lipids, and nucleic acids, leading to structural and functional changes that impair cellular functions. AGEs interact with receptors for AGEs (RAGE), altering intracellular signaling, gene expression, and pro-inflammatory responses. The glycation of plasma proteins like albumin, fibrinogen, globulins, and collagen leads to the formation of different AGEs, which play a key role in the pathogenesis of diabetic complications. AGEs are involved in oxidative stress, inflammation, and the development of diabetic complications through mechanisms such as altered enzyme activity, receptor dysfunction, and cross-linking of proteins. The Maillard reaction, a three-stage process, leads to the formation of AGEs, which are associated with aging and disease. Glycation of collagen and other proteins contributes to tissue stiffness, bone fragility, and vascular dysfunction. AGEs also contribute to the progression of diabetic complications by activating signaling pathways, increasing oxidative stress, and promoting inflammation. Pharmacological interventions targeting AGEs, such as pravastatin, GLP-1 receptor agonists, aminoguanidine, and curcumin, have shown beneficial effects in reducing diabetic complications. RAGE plays a central role in the pathogenesis of diabetic complications, and its inhibition may offer therapeutic potential. Overall, AGEs are a significant contributor to the development and progression of diabetic complications, and targeting their formation and signaling pathways may provide effective therapeutic strategies.Advanced glycation end products (AGEs) are formed through non-enzymatic glycation of proteins in diabetes, contributing to various complications such as retinopathy, nephropathy, neuropathy, and cardiomyopathy. AGEs form cross-links with proteins, lipids, and nucleic acids, leading to structural and functional changes that impair cellular functions. AGEs interact with receptors for AGEs (RAGE), altering intracellular signaling, gene expression, and pro-inflammatory responses. The glycation of plasma proteins like albumin, fibrinogen, globulins, and collagen leads to the formation of different AGEs, which play a key role in the pathogenesis of diabetic complications. AGEs are involved in oxidative stress, inflammation, and the development of diabetic complications through mechanisms such as altered enzyme activity, receptor dysfunction, and cross-linking of proteins. The Maillard reaction, a three-stage process, leads to the formation of AGEs, which are associated with aging and disease. Glycation of collagen and other proteins contributes to tissue stiffness, bone fragility, and vascular dysfunction. AGEs also contribute to the progression of diabetic complications by activating signaling pathways, increasing oxidative stress, and promoting inflammation. Pharmacological interventions targeting AGEs, such as pravastatin, GLP-1 receptor agonists, aminoguanidine, and curcumin, have shown beneficial effects in reducing diabetic complications. RAGE plays a central role in the pathogenesis of diabetic complications, and its inhibition may offer therapeutic potential. Overall, AGEs are a significant contributor to the development and progression of diabetic complications, and targeting their formation and signaling pathways may provide effective therapeutic strategies.