Targeting the AGEs-RAGE axis: pathogenic mechanisms and therapeutic interventions in diabetic wound healing

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Diabetes is a global health problem, with diabetic wounds constituting one of its most severe complications. Advanced glycation end products (AGEs) and their receptor, the receptor for advanced glycation end products (RAGE), play a key role in the pathogenesis of diabetic wounds. Accumulated AGEs bind to RAGE, activating various inflammatory and oxidative stress pathways such as NF-κB, PI3K-AKT, and JAK-STAT signaling, impairing normal wound healing. This review describes mechanisms by which the AGEs-RAGE axis disrupts vascular function, immune regulation, and cellular regeneration, thereby driving the formation of chronic non-healing wounds. Furthermore, we discuss emerging therapeutic strategies targeting the AGEs-RAGE axis, such as selective RAGE inhibitors, monoclonal antibodies, gene-based interventions, and AGE scavengers, highlighting their potential to enhance the treatment of diabetic chronic wounds.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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