Diabetic keratopathy is a significant ocular complication of diabetes mellitus (DM), affecting up to 70% of diabetic patients. It involves structural and functional changes in the cornea, including epithelial defects, reduced sensitivity, and delayed wound healing, leading to corneal ulcers, scarring, and opacities, which can cause irreversible vision loss. This review explores the pathomechanisms underlying diabetic keratopathy, focusing on redox signaling pathways and oxidative stress. Hyperglycemia contributes to the formation of advanced glycation end products (AGEs) and reactive oxygen species (ROS), which trigger inflammation, apoptosis, and fibrosis. These processes are mediated through pathways such as NF-κB, NLRP3 inflammasome, and the polyol pathway, leading to corneal nerve damage and dysfunction. Diabetic corneal neuropathy is characterized by reduced corneal sensitivity and impaired nerve conduction, contributing to dry eye disease (DED) and corneal epithelial defects. The review also highlights the role of oxidative stress in disrupting tear film stability and increasing the risk of infections. Experimental studies suggest that antioxidants such as vitamin D derivatives, α-lipoic acid, and Nrf2 activators may offer therapeutic potential in managing diabetic keratopathy by reducing oxidative stress, inflammation, and promoting corneal wound healing and nerve regeneration. Additionally, topical insulin and other compounds show promise in improving corneal epithelial defects and nerve repair. The review emphasizes the need for further clinical trials to validate the safety and efficacy of these therapeutic approaches in human patients.Diabetic keratopathy is a significant ocular complication of diabetes mellitus (DM), affecting up to 70% of diabetic patients. It involves structural and functional changes in the cornea, including epithelial defects, reduced sensitivity, and delayed wound healing, leading to corneal ulcers, scarring, and opacities, which can cause irreversible vision loss. This review explores the pathomechanisms underlying diabetic keratopathy, focusing on redox signaling pathways and oxidative stress. Hyperglycemia contributes to the formation of advanced glycation end products (AGEs) and reactive oxygen species (ROS), which trigger inflammation, apoptosis, and fibrosis. These processes are mediated through pathways such as NF-κB, NLRP3 inflammasome, and the polyol pathway, leading to corneal nerve damage and dysfunction. Diabetic corneal neuropathy is characterized by reduced corneal sensitivity and impaired nerve conduction, contributing to dry eye disease (DED) and corneal epithelial defects. The review also highlights the role of oxidative stress in disrupting tear film stability and increasing the risk of infections. Experimental studies suggest that antioxidants such as vitamin D derivatives, α-lipoic acid, and Nrf2 activators may offer therapeutic potential in managing diabetic keratopathy by reducing oxidative stress, inflammation, and promoting corneal wound healing and nerve regeneration. Additionally, topical insulin and other compounds show promise in improving corneal epithelial defects and nerve repair. The review emphasizes the need for further clinical trials to validate the safety and efficacy of these therapeutic approaches in human patients.