Diabetic vascular complications
Accumulation of advanced glycation end products on vascular and matrix proteins is a recognized mechanism contributing to the microvascular and macrovascular complications of chronic hyperglycemia.1
Glycome Atlas
concept
Also known as AGE, AGEs
Plain-language answer
Advanced glycation end products, often shortened to AGEs, are the permanent, browned compounds that form when sugars slowly react with proteins and stay stuck. They are the final product of a chain of reactions that begins when blood sugar attaches to a protein. Once formed, most of them cannot be undone, so they build up on tissues that turn over slowly.12
As advanced glycation end products accumulate, they stiffen and cross-link structural proteins and can trigger inflammation when they bind cell receptors. This buildup is linked to the aging of blood vessels and to complications of diabetes affecting the eyes, kidneys, nerves, and heart.1
Technical detail
Advanced glycation end products are a heterogeneous class of stable compounds generated in the late stages of the Maillard reaction through oxidation, dehydration, and cross-linking of Amadori products and reactive dicarbonyls with protein, lipid, and nucleic acid amino groups.1
Advanced glycation end products arise from Amadori products and from reactive dicarbonyl intermediates such as methylglyoxal and glyoxal. The resulting adducts range from non-cross-linking modifications of lysine and arginine, including carboxymethyllysine, to fluorescent cross-links that covalently tether adjacent protein chains. This chemical heterogeneity means the term denotes a family of structures rather than one defined molecule.1
Advanced glycation end products damage tissue through two broad routes. Cross-linking of long-lived extracellular matrix proteins such as collagen alters their mechanical properties and reduces turnover, while engagement of cell-surface receptors for advanced glycation end products activates pro-inflammatory and pro-oxidant signaling. Together these mechanisms are implicated in vascular stiffening and chronic diabetic complications.1
Human relevance
Accumulation of advanced glycation end products on vascular and matrix proteins is a recognized mechanism contributing to the microvascular and macrovascular complications of chronic hyperglycemia.1
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