ReviewInternational ophthalmology2025
Alterations of the ocular surface during diabetes: molecular mechanisms and therapeutic strategies.
Review in International ophthalmology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- GLP-1 Receptor Agonists and the Ocular Surface: A Narrative Review of Restoration, Remodeling, and Clinical Implications.Ophthalmology and therapy · 2026Review
- Paired Tear Fluid - Plasma Inflammatory Profiling Identifies Compartment-Specific Biomarkers for Diabetic Retinopathy and Diabetic Macular Edema.Journal of inflammation research · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
backgroundChronic hyperglycemia disrupts ocular surface homeostasis through oxidative stress, inflammation, autonomic neuropathy, and microvascular damage. These alterations contribute to dry eye disease, conjunctival changes, and corneal neuropathy, yet the underlying mechanisms are not fully understood. This review explores the molecular, cellular, and physiological pathways involved in diabetes-related ocular surface damage and summarizes current and emerging therapeutic approaches.
methodsA narrative review of peer-reviewed literature was performed, integrating clinical, histological, and molecular findings on conjunctival alterations, tear film dysfunction, oxidative stress, microbiota changes, and corneal nerve impairment in diabetic patients. Both established treatments and therapies under clinical or preclinical development were examined.
resultsHyperglycemia induces the accumulation of advanced glycation end-products, activates RAGE signaling, and increases ROS production, leading to endothelial dysfunction, goblet cell loss, and epithelial barrier compromise. Tear film instability results from lacrimal gland microvascular injury, Meibomian gland dysfunction, and reduced corneal sensitivity secondary to neuropathy. Corneal neuropathy-marked by reduced sub-basal nerve density, nerve tortuosity, punctate keratitis, and delayed healing-affects up to 70% of patients and may precede diabetic retinopathy. Treatments include lubricants, autologous serum, topical insulin, amniotic membranes, and tarsorrhaphy. Promising experimental therapies include neurotrophic factors, α-lipoic acid, PEDF, resolvins, GLP-1-based agents, and gene-based strategies.
conclusionDiabetes profoundly impacts the ocular surface through oxidative, inflammatory, neurogenic, and microvascular mechanisms that compromise tear film stability and corneal health. Early detection and targeted management are crucial to prevent progression to neurotrophic keratopathy. Further research is needed to refine mechanism-driven therapies.
Indexed as
Identifiers
41269387What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.