ArticleInternational journal of molecular medicine2016
Involvement of NADPH oxidases in alkali burn-induced corneal injury.
Article in International journal of molecular medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
28 citing papers in PubMed, 52 citations in OpenAlex.
- Chrysin Attenuates Dry Eye Progression by Suppressing NOX2-Dependent Ferroptosis and STING/NLRP3-Mediated Inflammatory Responses.Investigative ophthalmology & visual science · 2026Article
- Chiglitazar Activates PPAR-α/γ to Suppress Oxidative Stress and Angiogenesis in Corneal Neovascularization.Antioxidants (Basel, Switzerland) · 2026Article
- Celastrol nanomedicine eye drops restore redox homeostasis and prevents keratoconus progression via PI3K/AKT/AP-1 signaling.Redox biology · 2026Article
- The efficacy of bone marrow-derived mesenchymal stem cells in restoring limbal stem cell deficiency in rat model.Scientific reports · 2025Article
- Transforming corneal alkali burn treatment: unveiling mechanisms and pioneering therapies from bench to bedside.Journal of translational medicine · 2025Review
- Rapamycin Mitigates Corneal Damage in a Mouse Model of Alkali Burn Injury.Bioengineering (Basel, Switzerland) · 2025Article
- The Role of Connexin 36 Gap Junctions in Retinal Ganglion Cell Death After Corneal Alkali Burns.Investigative ophthalmology & visual science · 2025Article
- Efficacy and safety of Fe-curcumin coordination polymer nanodots to prevent corneal neovascularization in alkali burn models.Journal of nanobiotechnology · 2025Article
- NADPH oxidases: redox regulation of cell homeostasis and disease.Physiological reviews · 2025Review
- Isolated Mitochondrial Transplantation as a Novel Treatment for Corneal Chemical Burns.Investigative ophthalmology & visual science · 2025Article
- LSD1 inhibition by tranylcypromine hydrochloride reduces alkali burn-induced corneal neovascularization and ferroptosis by suppressing HIF-1α pathway.Frontiers in pharmacology · 2024Article
- Composite Hydrogel Modulates Intrinsic Immune-Cascade Neovascularization for Ocular Surface Reconstruction after Corneal Chemical Injury.Gels (Basel, Switzerland) · 2023Article
- Comparison of Corneal Epithelial Wound Healing between Topical RCI001, Solcoseryl, and Polydeoxyribonucleotide in the Murine Ocular Alkali Burn Model.Korean journal of ophthalmology : KJO · 2023Article
- Pathogenesis of Alkali Injury-Induced Limbal Stem Cell Deficiency: A Literature Survey of Animal Models.Cells · 2023Review
- A Rational Design of Metal-Organic Framework Nanozyme with High-Performance Copper Active Centers for Alleviating Chemical Corneal Burns.Nano-micro letters · 2023Article
- Functional Peptide-Loaded Gelatin Nanoparticles as Eyedrops for Cornea Neovascularization Treatment.International journal of nanomedicine · 2023Article
- Article
- Concentration-associated pathology of alkali burn in a mouse model using anterior segment optical coherence tomography with angiography.Experimental eye research · 2022Article
- AIP1 suppresses neovascularization by inhibiting the NOX4-induced NLRP3/NLRP6 imbalance in a murine corneal alkali burn model.Cell communication and signaling : CCS · 2022Article
- Seawater immersion exacerbates the pathological changes caused by incisive corneal injury in rabbit eyes.Annals of translational medicine · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chemical burns are a major cause of corneal injury. Oxidative stress, inflammatory responses and neovascularization after the chemical burn aggravate corneal damage, and lead to loss of vision. Although NADPH oxidases (Noxs) play a crucial role in the production of reactive oxygen species (ROS), the role of Noxs in chemical burn-induced corneal injury remains to be elucidated. In the present study, the transcription and expression of Noxs in corneas were examined by RT-qPCR, western blot analysis and immunofluorescence staining. It was found that alkali burns markedly upregulated the transcription and expression of Nox2 and Nox4 in human or mouse corneas. The inhibition of Noxs by diphenyleneiodonium (DPI) or apocynin (Apo) effectively attenuated alkali burn-induced ROS production and decreased 3-nitrotyrosine (3-NT) protein levels in the corneas. In addition, Noxs/CD11b double‑immunofluorescence staining indicated that Nox2 and Nox4 were partially co-localized with CD11b. DPI or Apo prevented the infiltration of CD11b-positive inflammatory cells, and inhibited the transcription of inflammatory cytokines following alkali burn-induced corneal injury. In our mouse model of alkali burn-induced corneal injury, corneal neovascularization (CNV) occurred on day 3, and it affected 50% of the whole area of the cornea on day 7, and on day 14, CNV coverage of the cornea reached maximum levels. DPI or Apo effectively attenuated alkali burn‑induced CNV and decreased the mRNA levels of angiogenic factors, including vascular endothelial growth factor (VEGF), VEGF receptors and matrix metalloproteinases (MMPs). Taken together, our data indicate that Noxs play a role in alkali burn-induced corneal injury by regulating oxidative stress, inflammatory responses and CNV, and we thus suggest that Noxs are a potential therapeutic target in the future treatment of chemical-induced corneal injury.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.