Advanced glycation end products || AGE || Diabetics

Advanced glycation end products || AGE
Advanced glycation end products (AGEs) are proteins or lipids that become glycated after exposure to sugars. AGEs are prevalent in the diabetic vasculature and contribute to the development of atherosclerosis. The presence and accumulation of AGEs in many different cell types affect extracellular and intracellular structure and function. AGEs contribute to a variety of microvascular and macrovascular complications through the formation of cross-links between molecules in the basement membrane of the extracellular matrix and by engaging the receptor for advanced glycation end products (RAGE). Activation of RAGE by AGEs causes upregulation of the transcription factor nuclear factor-κB and its target genes. Soluble AGEs activate monocytes, and AGEs in the basement membrane inhibit monocyte migration. AGE-bound RAGE increases endothelial permeability to macromolecules. AGEs block nitric oxide activity in the endothelium and cause the production of reactive oxygen species. Because of the emerging evidence about the adverse effects of AGEs on the vasculature of patients with diabetes, a number of different therapies to inhibit AGEs are under investigation.

Advanced glycation end products (AGEs) are modifications of proteins or lipids that become nonenzymatically glycated and oxidized after contact with aldose sugars.1,2 Early glycation and oxidation processes result in the formation of Schiff bases and Amadori products. Further glycation of proteins and lipids causes molecular rearrangements that lead to the generation of AGEs.1 AGEs may fluoresce, produce reactive oxygen species (ROS), bind to specific cell surface receptors, and form cross-links.1,3 AGEs form in vivo in hyperglycemic environments and during aging and contribute to the pathophysiology of vascular disease in diabetes.4–7 This review summarizes AGE formation and biochemistry, cellular receptors for AGE, AGE-induced effects on extracellular and intracellular functions, and developing AGE therapies.

AGEs accumulate in the vessel wall, where they may perturb cell structure and function. AGEs have been implicated in both the microvascular and macrovascular complications of diabetes. As reviewed by Brownlee,5 AGEs may modify the extracellular matrix (ECM); modify the action of hormones, cytokines, and free radicals via engagement of cell surface receptors; and impact the function of intracellular proteins.
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