ArticlePloS one2021
Pathophysiology and inflammatory biomarkers of sulfur mustard-induced corneal injury in rabbits.
Article in PloS one, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
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.
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Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.
- A Systematic Review of Tear Vascular Endothelial Growth Factor and External Eye Diseases.International journal of molecular sciences · 2024Pooled it
- Dexamethasone alters the cornea transcriptome to confer protection against ocular sulfur mustard exposure via regulating NFκB and TGFβ signaling in an in vivo rabbit model.Archives of toxicology · 2026Article
- Predicting the severity of eye damage induced in rabbits after sulfur mustard vapor exposure.Toxicology reports · 2025Article
- Current progress in research on ocular injury caused by exposure to vesicants.Progress in retinal and eye research · 2025Review
- Unveiling the acute toxic pathology and transcriptomic signature of ocular exposure to phosgene oxime using an in vivo mouse model: A novel pilot study.Toxicology and applied pharmacology · 2025Article
- Dexamethasone mitigates sulfur mustard-induced stem cell deficiency in vivo in rabbit limbal tissue by reducing inflammation and oxidative stress.Archives of toxicology · 2025Article
- Article
- Dexamethasone sodium phosphate loaded nanoparticles for prevention of nitrogen mustard induced corneal injury.Experimental eye research · 2024Article
- Chloropicrin induced ocular injury: Biomarkers, potential mechanisms, and treatments.Toxicology letters · 2024Review
- Dexamethasone targets actin cytoskeleton signaling and inflammatory mediators to reverse sulfur mustard-induced toxicity in rabbit corneas.Toxicology and applied pharmacology · 2024Article
- Nitrogen Mustard-Induced Ex Vivo Human Cornea Injury Model and Therapeutic Intervention by Dexamethasone.The Journal of pharmacology and experimental therapeutics · 2024Article
- Establishing a Dexamethasone Treatment Regimen To Alleviate Sulfur Mustard-Induced Corneal Injuries in a Rabbit Model.The Journal of pharmacology and experimental therapeutics · 2024Article
- Phenylarsine oxide induced corneal injury involves oxidative stress mediated unfolded protein response and ferroptotic cell death: Amelioration by NAC.Free radical biology & medicine · 2023Article
- Insights into mustard gas keratopathy- characterizing corneal layer-specific changes in mice exposed to nitrogen mustard.Experimental eye research · 2023Article
- Metabolomics for identifying pathways involved in vesicating agent lewisite-induced corneal injury.Experimental eye research · 2023Article
- Cellular senescence implication in mustard keratopathy.Experimental eye research · 2023Article
- Mustard gas exposure instigates retinal Müller cell gliosis.Experimental eye research · 2023Article
- Ocular injury progression and cornea histopathology from chloropicrin vapor exposure: Relevant clinical biomarkers in mice.Experimental eye research · 2023Article
- Role of aquaporins in corneal healing post chemical injury.Experimental eye research · 2023Review
- Progress towards a standardized model of ocular sulfur mustard injury for therapeutic testing.Experimental eye research · 2023Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Sulfur mustard (SM) is a cytotoxic, vesicating, chemical warfare agent, first used in 1917; corneas are particularly vulnerable to SM exposure. They may develop inflammation, ulceration, neovascularization (NV), impaired vision, and partial/complete blindness depending upon the concentration of SM, exposure duration, and bio-physiological conditions of the eyes. Comprehensive in vivo studies have established ocular structural alterations, opacity, NV, and inflammation upon short durations (<4 min) of SM exposure. In this study, detailed analyses of histopathological alterations in corneal structure, keratocytes, inflammatory cells, blood vessels, and expressions of cyclooxygenase (COX)-2, matrix metalloproteinase (MMP)-9, vascular endothelial growth factor (VEGF), and cytokines were performed in New Zealand white rabbits, in a time-dependent manner till 28 days, post longer durations (5 and 7 min) of ocular SM exposure to establish quantifiable endpoints of injury and healing. Results indicated that SM exposure led to duration-dependent increases in corneal thickness, opacity, ulceration, epithelial-stromal separation, and epithelial degradation. Significant increases in NV, keratocyte death, blood vessels, and inflammatory markers (COX-2, MMP-9, VEGF, and interleukin-8) were also observed for both exposure durations compared to the controls. Collectively, these findings would benefit in temporal delineation of mechanisms underlying SM-induced corneal toxicity and provide models for testing therapeutic interventions.
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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.