ArticleActa pharmacologica Sinica2019
Diabetes inhibits corneal epithelial cell migration and tight junction formation in mice and human via increasing ROS and impairing Akt signaling.
Article in Acta pharmacologica Sinica, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.
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Who cites it
41 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.
- Exploring the Role of GLP-1 Agents in Managing Diabetic Foot Ulcers: A Narrative and Systematic Review.Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair SocietyPooled it
- Study on the Regulatory Mechanism of GLP-1 Receptor Agonist Liraglutide in Diabetic Corneal Epithelial Wound Healing.Investigative ophthalmology & visual science · 2026Article
- ROS-Responsive Eye Drop for Controlled Release of 20-Deoxyingenol Improves Diabetic Corneal Healing by Activating Macrophage Autophagy and Metabolic Reprogramming.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Evaluation of dECM hydrogel-NAP on 3D organotypic human corneal epithelium in diabetic keratopathy model.Scientific reports · 2026Article
- Oxidative stress-regulatory role of miR-10b-5p in the diabetic human cornea revealed through integrated multi-omics analysis.Diabetologia · 2026Article
- Article
- Umbelliferone preserves skin epidermal barrier integrity in diabetes-induced keratinocytes by regulating actin dynamics and suppressing ROS-mediated apoptosis.Nutrition & diabetes · 2025Article
- Beyond the Surface: Revealing the Concealed Effects of Hyperglycemia on Ocular Surface Homeostasis and Dry Eye Disease.Medicina (Kaunas, Lithuania) · 2025Review
- Glucosamine mitigates hyperglycemic-induced oxidative stress via the SIRT1 pathway in human corneal epithelial cells.Scientific reports · 2025Article
- DJ-1 Promotes Diabetic Corneal Epithelial Wound Healing by Attenuating Hyperglycemia-Induced Oxidative Stress Through Inhibiting PTEN.Investigative ophthalmology & visual science · 2025Article
- CXCL12 as a Potential Hub Gene for N-Acetylcysteine Treatment of T1DM Liver Disease.Biomolecules · 2025Article
- AI-driven strategies for advancing corneal cell therapy: a promising frontier.Frontiers in medicine · 2025Review
- The Role of Immune Cells and Signaling Pathways in Diabetic Eye Disease: A Comprehensive Review.Biomedicines · 2024Review
- Optical microsensing reveals spatiotemporal oxygen dynamics in cornea wounds that affect healing via reactive oxygen species.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- Topical and oral peroxisome proliferator-activated receptor-α agonist ameliorates diabetic corneal neuropathy.Scientific reports · 2024Article
- Top Five Stories of the Cellular Landscape and Therapies of Atherosclerosis: Current Knowledge and Future Perspectives.Current medical science · 2024Review
- Diabetic Keratopathy: Redox Signaling Pathways and Therapeutic Prospects.Antioxidants (Basel, Switzerland) · 2024Review
- Article
- The role of Q10 engineering mesenchymal stem cell-derived exosomes in inhibiting ferroptosis for diabetic wound healing.Burns & trauma · 2024Article
- Hyperglycemia causes differential change in macrophage population in the lacrimal gland, conjunctiva and cornea.Frontiers in immunology · 2024Article
Corrections and comments
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Authors and funding
12 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Corneal wounds usually heal quickly; but diabetic patients have more fragile corneas and experience delayed and painful healing. In the present study, we compared the healing capacity of corneal epithelial cells (CECs) between normal and diabetic conditions and the potential mechanisms. Primary murine CEC derived from wild-type and diabetic (db/db) mice, as well as primary human CEC were prepared. Human CEC were exposed to high glucose (30 mM) to mimic diabetic conditions. Cell migration and proliferation were assessed using Scratch test and MTT assays, respectively. Reactive oxygen species (ROS) production in the cells was measured using dichlorofluorescein reagent. Western blot was used to evaluate the expression levels of Akt. Transepithelial electrical resistance (TEER) and zonula occludens-1 (ZO-1) expression were used to determine tight junction integrity. We found that the diabetic CEC displayed significantly slower cell proliferation and migration compared with the normal CEC from both mice and humans. Furthermore, ROS production was markedly increased in CEC grown under diabetic conditions. Treatment with an antioxidant N-acetyl cysteine (NAC, 100 μM) significantly decreased ROS production and increased wound healing in diabetic CEC. Barrier function was significantly reduced in both diabetic mouse and human CEC, while NAC treatment mitigated these effects. We further showed that Akt signaling was impaired in diabetic CEC, which was partially improved by NAC treatment. These results show that diabetic conditions lead to delayed wound-healing capacity of CEC and impaired tight junction formation in both mice and human. Increased ROS production and inhibited Akt signaling may contribute to this outcome, implicating these as potential targets for treating corneal wounds in diabetic patients.
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