ArticleFrontiers in medicine2026
Investigating the shared genetic architecture between dry eye disease and multisite chronic pain.
Article in Frontiers in medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: The epidemiological link between dry eye disease (DED) and chronic pain is established, yet a shared genetic etiology remains uncertain. Methods: Utilizing GWAS summary data, we applied linkage disequilibrium score regression (LDSC) to determine genetic correlation between DED and multisite chronic pain (MCP). We investigated SNP enrichment across tissues using stratified LD score regression (S-LDSC) and multimarker analysis of genome annotation (MAGMA). Common risk SNPs were identified via Multi-Trait Analysis of GWAS (MTAG) and Cross-Phenotype Association (CPASSOC), followed by pleiotropic analysis under the composite null hypothesis (PLACO) and colocalization. Multi-trait colocalization (Hyprcoloc) integrating brain imaging-derived phenotypes (IDPs) was applied to explore neuroimaging mediators. We further investigated risk gene expression profiles using Summary-data-based Mendelian randomization (SMR) to explore functional genes. Results: We found significant genetic correlation between DED and MCP, highlighting shared risk SNPs (rs13107325, rs7105462, rs7959961). Hyprcoloc revealed rs13107325 as a central hub with three-way colocalization across 95 IDPs. Partitioned analysis identified 11 functional elements associated with both phenotypes. Tissue enrichment converged on brain regions, notably the anterior cingulate cortex and cerebellar hemispheres. SMR identified 21 shared functional genes. Conclusion: This study suggests genetic correlation and common risk genes between DED and MCP, advancing understanding of their pathogenesis and assisting in identifying therapeutic targets.
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.