ArticleBiomolecules2023
Lipoxin A4 (LXA4) Reduces Alkali-Induced Corneal Inflammation and Neovascularization and Upregulates a Repair Transcriptome.
Article in Biomolecules, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 12 citations in OpenAlex.
- When LXA4 meets white fat: browning via the miR-133a-3p/SIRT1 pathway in mouse models.Adipocyte · 2026Article
- Specialized Pro-Resolving Mediators at the Ocular Surface: Biosynthesis, Mechanisms, and Therapeutic Potential.Biology · 2026Review
- Lipoxin A 4 (LXA 4 ) for diabetic retinopathy (DR).Indian journal of ophthalmology · 2026Article
- Resolvin D1 requires TLR2-FPR2 crosstalk for inflammation resolution and protection during ocular bacterial infection.Communications biology · 2026Article
- Transforming corneal alkali burn treatment: unveiling mechanisms and pioneering therapies from bench to bedside.Journal of translational medicine · 2025Review
- Lipoxins as Modulators of Diseases.Cells · 2025Review
- Efficacy and safety of Fe-curcumin coordination polymer nanodots to prevent corneal neovascularization in alkali burn models.Journal of nanobiotechnology · 2025Article
- Lipoxin A4 (LXA4) as a Potential Drug for Diabetic Retinopathy.Medicina (Kaunas, Lithuania) · 2025Review
- A new R,R-RvD6 isomer with protective actions following corneal nerve injury.Prostaglandins & other lipid mediators · 2024Review
- Supersaturated Oxygen Emulsion Mitigates Hypoxia-Driven Corneal Neovascularization after Alkali Burn.Ophthalmology scienceArticle
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
purposeTo investigate the anti-inflammatory and anti-angiogenic effects of the bioactive lipid mediator LXA4 on a rat model of severe corneal alkali injury.
methodsTo induce a corneal alkali injury in the right eyes of anesthetized Sprague Dawley rats. They were injured with a Φ 4 mm filter paper disc soaked in 1 N NaOH placed on the center of the cornea. After injury, the rats were treated topically with LXA4 (65 ng/20 μL) or vehicle three times a day for 14 days. Corneal opacity, neovascularization (NV), and hyphema were recorded and evaluated in a blind manner. Pro-inflammatory cytokine expression and genes involved in cornel repair were assayed by RNA sequencing and capillary Western blot. Cornea cell infiltration and monocytes isolated from the blood were analyzed by immunofluorescence and by flow cytometry.
resultsTopical treatment with LXA4 for two weeks significantly reduced corneal opacity, NV, and hyphema compared to the vehicle treatment. RNA-seq and Western blot results showed that LXA4 decreased the gene and protein expression of pro-inflammatory cytokines interleukin (IL)-1β and IL-6 and pro-angiogenic mediators matrix metalloproteinase (MMP)-9 and vascular endothelial growth factor (VEGFA). It also induces genes involved in keratinization and ErbB signaling and downregulates immune pathways to stimulate wound healing. Flow cytometry and immunohistochemistry showed significantly less infiltration of neutrophils in the corneas treated with LXA4 compared to vehicle treatment. It also revealed that LXA4 treatment increases the proportion of type 2 macrophages (M2) compared to M1 in blood-isolated monocytes.
conclusionsLXA4 decreases corneal inflammation and NV induced by a strong alkali burn. Its mechanism of action includes inhibition of inflammatory leukocyte infiltration, reduction in cytokine release, suppression of angiogenic factors, and promotion of corneal repair gene expression and macrophage polarization in blood from alkali burn corneas. LXA4 has potential as a therapeutic candidate for severe corneal chemical injuries.
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Registered trials
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