The aim is to explore how advanced glycation end-products affect corneal wound healing in diabetes.
Investigated the role of AGE/TLR4 signaling in corneal epithelial cells.
Analyzed the activation of inflammatory pathways, including p65 and IRF3.
Examined the relationship between AGE levels and diabetic keratopathy progression.
AGE/TLR4 signaling was found to sustain corneal inflammation.
Activation of p65 and IRF3 was linked to delayed wound healing.
Identified AGE/TLR4 signaling as a key target for therapeutic intervention in diabetic keratopathy.
Abstract
The AGE/TLR4 axis drives sustained corneal inflammation by activating p65 and IRF3, thereby promoting DK progression. These findings identify AGE/TLR4 signaling as a potential therapeutic target for DK.