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Advanced glycation end-products (AGEs) are heterogeneous molecules resulting from the non-enzymatic glycation and oxidation of proteins, lipids, and nucleic acids by reducing sugars, a process accelerated under hyperglycemic conditions and during aging[3][1][7]. AGEs can be formed endogenously or absorbed from the diet, especially from foods cooked at high temperatures[3][8]. The accumulation of AGEs alters the structure and function of long-lived molecules (such as collagen), contributes to cross-link formation, increases oxidative stress and inflammation, and engages cell surface receptors such as RAGE (receptor for advanced glycation end-products), leading to downstream signaling cascades implicated in the development and progression of diabetes complications, cardiovascular disease, neurodegeneration, and other age-related disorders[1][2][3][7][4][8]. Targeting AGE accumulation or its downstream pathways is a therapeutic strategy under investigation, but AGEs themselves are not a single pharmacological target[3][7][1].
AGE inhibitors (inhibit formation of AGEs), AGE breakers (cleave AGE crosslinks), AGE receptor antagonists (block signaling, e.g., anti-RAGE antibodies), Glyoxalase system activators (increase degradation of AGE precursors)
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