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AGEs primarily exert their pathological effects by trapping and crosslinking the protein or by interacting with their receptor RAGE, triggering oxidative stress, inflammatory responses, and apoptosis, which further exacerbate tissue and organ damage

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It has been suggested that this PTM of the mitochondrial proteins enables the recruitment of the autophagy adaptor p62, leading to the autophagosomal degradation of the damaged mitochondria [12, 278, 279]