ArticleThe American journal of pathology2017
Mechanisms of Retinal Damage after Ocular Alkali Burns.
Article in The American journal of pathology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 2 of them syntheses that pooled it.
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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.
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Who cites it
55 citing papers in PubMed, 2 syntheses or guidelines pooled it, 86 citations in OpenAlex.
- Retinal changes and treatment in ocular alkali burn: a systematic review of animal models and case reports summary.BMC ophthalmology · 2026Pooled it
- The pivotal role of inflammatory factors in glaucoma: a systematic review.Frontiers in immunology · 2025Pooled it
- BRD4 inhibition mitigates acute and chronic corneal injury following topical nitrogen mustard exposure.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- Artificial Intelligence for In-Flight Detection of Space-Related Ocular Trauma: Bridging Diagnostic Gaps in Microgravity.Vision (Basel, Switzerland) · 2026Review
- [Research progress and applications of biologically derived materials in scleral reconstruction].Zhongguo xiu fu chong jian wai ke za zhi = Zhongguo xiufu chongjian waike zazhi = Chinese journal of reparative and reconstructive surgery · 2026Review
- Effect of Powder-to-Liquid Ratio on pH, Calcium Ion Release, and Solubility Behaviors of Endodontic Bioceramics: An In Vitro Study.Journal of functional biomaterials · 2026Article
- Intermediate Term Results of a Novel Minimally Invasive Keratoprosthesis.Ophthalmology science · 2026Article
- Evaluation of the Physicochemical and Biological Properties of Calcium-Silicate-Based Root-End Filling Materials.Journal of functional biomaterials · 2026Article
- Current progress in research on ocular injury caused by exposure to vesicants.Progress in retinal and eye research · 2025Review
- Transforming corneal alkali burn treatment: unveiling mechanisms and pioneering therapies from bench to bedside.Journal of translational medicine · 2025Review
- The Role of Connexin 36 Gap Junctions in Retinal Ganglion Cell Death After Corneal Alkali Burns.Investigative ophthalmology & visual science · 2025Article
- Changes in Retinal Nerve Fiber and Ganglion Cell Layers After Chemical Injury: A Prospective Study.Journal of clinical medicine · 2025Article
- Epigenetic Adaptation Drives Monocyte Differentiation into Microglia-Like Cells Upon Engraftment into the Central Nervous System.bioRxiv : the preprint server for biology · 2025Article
- RIPK3-Mediated Necroptosis Drives Macrophage Infiltration and Corneal Neovascularization After Alkali Burn.Investigative ophthalmology & visual science · 2025Article
- Article
- International Harmonization of Nomenclature and Diagnostic Criteria (INHAND): Nonproliferative and Proliferative Lesions of Nonrodent Ocular Tissues.Toxicologic pathology · 2024Review
- The prophylactic value of TNF-α inhibitors against retinal cell apoptosis and optic nerve axon loss after corneal surgery or trauma.Acta ophthalmologica · 2024Article
- Alkali injury-induced pathological lymphangiogenesis in the iris facilitates the infiltration of T cells and ocular inflammation.JCI insight · 2024Article
- Influence of topical NPH-insulin use on wound healing and oxidative stress in alkali corneal burns: an experimental study in a rabbit model.Iranian journal of veterinary research · 2024Article
- Efficient ocular delivery of siRNAInternational journal of pharmaceutics: X · 2023Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 2 countries.
Funding
Abstract
Alkali burns to the eye constitute a leading cause of worldwide blindness. In recent case series, corneal transplantation revealed unexpected damage to the retina and optic nerve in chemically burned eyes. We investigated the physical, biochemical, and immunological components of retinal injury after alkali burn and explored a novel neuroprotective regimen suitable for prompt administration in emergency departments. Thus, in vivo pH, oxygen, and oxidation reduction measurements were performed in the anterior and posterior segment of mouse and rabbit eyes using implantable microsensors. Tissue inflammation was assessed by immunohistochemistry and flow cytometry. The experiments confirmed that the retinal damage is not mediated by direct effect of the alkali, which is effectively buffered by the anterior segment. Rather, pH, oxygen, and oxidation reduction changes were restricted to the cornea and the anterior chamber, where they caused profound uveal inflammation and release of proinflammatory cytokines. The latter rapidly diffuse to the posterior segment, triggering retinal damage. Tumor necrosis factor-α was identified as a key proinflammatory mediator of retinal ganglion cell death. Blockade, by either monoclonal antibody or tumor necrosis factor receptor gene knockout, reduced inflammation and retinal ganglion cell loss. Intraocular pressure elevation was not observed in experimental alkali burns. These findings illuminate the mechanism by which alkali burns cause retinal damage and may have importance in designing therapies for retinal protection.
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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 OpenQuestion graph.