A Plant Photoregulator‐Inspired S‐Type Heterojunction System for Diabetic Keratopathy via Tri‐Modal Light‐Driven Immunometabolic Reprogramming, Tissue Repair, and Antibacterial Activity

ABSTRACT

Diabetic keratopathy (DK) is a prevalent ocular surface complication of diabetes, frequently unnoticed until significant structural and functional deterioration occurs. Chronic hyperglycemic stress promotes inflammation in the corneal epithelial‐neural‐immune (epineuroimmune) unit, impeding tissue recovery and increasing infection susceptibility. To address this metabolic–immune–infection imbalance, we developed a light‐regulated biomimetic catalytic platform (WCN _x ‐Rh2) that integrates glucose degradation and monitoring, immune‐modulated epithelial‐neural regeneration, and antibacterial defense. This platform features an S‐scheme heterojunction (WCN _x ) composed of graphitic carbon nitride and tungsten oxide, enabling visible‐light (VIS)‐driven glucose degradation, dark‐state colorimetric detection, and near‐infrared (NIR) photothermal antibacterial activity. Complementarily, the loaded ginsenoside Rh2—identified via systematic screening—inhibits the Nucleotide‐binding and oligomerization domain (NOD)‐like receptor signaling pathway. The combined action of WCN _x and Rh2 reduces advanced glycation end products (AGEs), reactive oxygen species (ROS), and inflammatory signaling, reprogramming dendritic cell function to restore epineuroimmune homeostasis and drive tissue repair. These functions were validated in two animal models. In diabetic mice, VIS‐irradiated WCN _x ‐Rh2 accelerated corneal epithelial and nerve recovery. In a diabetic keratitis model, NIR‐activated WCN _x ‐Rh2 enabled effective corneal bacterial eradication and tissue repair. Overall, this work establishes a light‐driven metabolic‐modulation biomimetic paradigm and proposes an integrated strategy for managing DK.