Diabetes-related ocular changes highlight rising concern for neurotrophic keratopathy

A new narrative review highlights how chronic hyperglycemia drives oxidative, inflammatory, and microvascular changes that damage the ocular surface, with particular concern for their role in neurotrophic keratopathy (NK).

The review describes how advanced glycation end-products, RAGE activation, and excess ROS weaken endothelial function, reduce goblet cells, and disrupt the epithelial barrier. Microvascular injury to the lacrimal and Meibomian glands, paired with reduced corneal sensitivity from diabetic neuropathy, further destabilizes the tear film.

Corneal neuropathy, which is marked by reduced sub-basal nerve density, nerve tortuosity, punctate keratitis, and delayed wound healing, affects up to 70% of people with diabetes and may precede retinopathy. These early nerve changes set the stage for NK, making timely detection critical.

Current therapies include lubricants, autologous serum, topical insulin, amniotic membranes, and tarsorrhaphy. Emerging strategies such as neurotrophic factors, α-lipoic acid, PEDF, resolvins, GLP-1–based agents, and gene-targeted approaches aim to better protect or regenerate corneal nerves.

The authors conclude that early recognition and mechanism-driven management are key to preventing progression to NK in diabetic patients.

Reference
Quintana-Pérez JC, Tamay-Cach F, Guillen-Castro SA, et al. Alterations of the ocular surface during diabetes: molecular mechanisms and therapeutic strategies. Int Ophthalmol. 2025;46(1):3. doi: 10.1007/s10792-025-03865-z. PMID: 41269387.