ArticleJournal of ophthalmology2026
Anti-Inflammatory Cytokine Signatures in Primary Glaucoma Subtypes: Diagnostic and Pathophysiological Insights From IL-36Ra, IL-37, and IL-38.
Article in Journal of ophthalmology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
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Who cites it
1 citing paper in PubMed.
- Anti-Inflammatory Cytokine Signatures in Primary Glaucoma Subtypes: Diagnostic and Pathophysiological Insights From IL-36Ra, IL-37, and IL-38.Journal of ophthalmology · 2026Article
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objectives: To quantify interleukin-36 receptor antagonist (IL-36Ra), interleukin-37 (IL-37), and interleukin-38 (IL-38) levels in aqueous humor and plasma of patients with primary glaucoma, and investigate their correlations with glaucomatous structural damage. Methods: Matched aqueous humor and plasma samples were collected from patients with acute primary angle-closure glaucoma (APACG), chronic PACG (CPACG), and primary open-angle glaucoma (POAG), and age-related cataract controls (ARC). Levels of IL-36Ra, IL-37, and IL-38 were quantified and correlated with average retinal nerve fiber layer thickness (RNFLT). Results: A total of 96 participants were enrolled, including 25 APACG, 23 CPACG, 23 POAG, and 25 ARC. In aqueous humor, IL-36Ra was significantly elevated in CPACG compared to all other groups, while IL-37 and IL-38 were markedly increased in both CPACG and POAG compared to ARC and APACG (all Conclusion: Aqueous humor IL-38 levels correlated with RNFLT thinning in POAG and CPACG, suggesting a potential role as a biomarker associated with structural damage. IL-36Ra was independently elevated in CPACG, supporting its potential as a subtype-related biomarker. Further studies are needed to clarify the mechanisms of these cytokines in glaucoma pathogenesis.
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