ArticleTranslational vision science & technology2025
Genetics of Circulating Inflammatory Proteins and Iridocyclitis: An Exploratory Mendelian Randomization Study.
Article in Translational vision science & technology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
- Causal effects of antibody-mediated immunity to pathogens on five ophthalmic diseases: a Mendelian randomization study.Experimental biology and medicine (Maywood, N.J.) · 2026Article
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Authors and funding
6 authors.
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Abstract
Purpose: This study aimed to explore the potential causal relationship between genetically determined elevated levels of pro-inflammatory cytokines and iridocyclitis, including its subtypes: acute and subacute iridocyclitis (ASIR) and chronic iridocyclitis (CIR). Methods: A two-sample Mendelian randomization (MR) analysis was conducted using genome-wide association study (GWAS) summary data for inflammatory cytokines (cases, n = 14,824), iridocyclitis (IR; cases, n = 7306 and controls, n = 357,814), and its subtypes (ASIR: cases, n = 6166 and controls, n = 357,814; and CIR: cases, n = 1401 and controls, n = 357,814). The inverse variance-weighted (IVW) method served as the primary analysis method. Supplementary analytic methods included MR Egger, Weighted median, Weighted mode, and Simple mode methods. Pleiotropy and heterogeneity were evaluated using the Cochran's Q test, MR Egger intercept test, MR Pleiotropy RESidual Sum and Outlier test (MR-PRESSO), Bayesian colocalization analysis, and Linkage disequilibrium score regression (LDSC) analysis. Results: Genetically predicted high levels of eotaxin, fibroblast growth factor 23 (FGF23), TNF-related apoptosis-inducing ligand (TRAIL), and Neurotrophin-3 were associated with an increased risk of IR. On the contrary, a high level of interleukin (IL)-2 was associated with a decreased risk of IR. Meanwhile, the IR subgroup analysis demonstrated that high levels of eotaxin and TRAIL were also associated with an increased risk of ASIR. High levels of cystatin D, tumor necrosis factor receptor superfamily member 9 (TNFRSF9), and caspase 8 were associated with an increased risk of CIR. CCL20 and CDCP1 were associated with a decreased risk of CIR. Heterogeneity and pleiotropy tests demonstrated that our findings were stable and reliable. Conclusions: Inflammatory cytokines are involved in the occurrence of IR and its subtypes. Further studies are warranted to elucidate the precise mechanisms of inflammatory cytokines in IR and its subtypes. Translational Relevance: The present study highlighted the role of inflammatory cytokines in the development of IR.
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