Abstract
Advanced glycation end-products (AGEs) are usually formed slowly under physiological conditions. The accumulation of AGEs increases with variable pathologies such as type 2 diabetes, cardiovascular disease (CVD), and aging (1, 2). The effect of AGEs is classified as receptorindependent (such as cross-links with extracellular matrix) or receptor-dependent. The binding of AGEs to the cellular receptor (receptor for AGE [RAGE]) activates members of the MAPK family of signal transduction effectors, including p44/42 MAPK, c-Jun N-terminal kinases MAPK, and p38 MAPK.Furthermore,AGE-RAGEinteractionstimulatesactivation of p21, Janus kinase/signal transducer and activator of transcription pathways, cdc42 and rac-1, Akt, and glycogen synthase kinase-3 signaling. These signaling pathwaysconvergeonmultiple transcription factors suchasearly growth response-1, nuclear factorB (NFB), and cyclic AMP response element-binding protein, which mediate alterations in cell fate, migration, and production of inflammatory and profibrotic mediators by increasing expression of cytokines, chemokines, and adhesion molecules. On the other hand, the binding of AGEs to the soluble receptor (sRAGE) prevents the adverse intracellular events of the AGE-RAGE system (2).
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