ArticleFrontiers in immunology2026
Multi-omics Mendelian randomization integrating GWAS, eQTL, mQTL and pQTL data prioritizes mitochondrial gene
Article in Frontiers in immunology, 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
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Mitochondrial dysfunction is linked to urolithiasis, but causal genetic drivers remain unclear. We integrated multi-omics data using Mendelian randomization to identify mitochondrial-related genes causally associated with urolithiasis. Methods: We obtained mitochondrial methylation (mQTL), gene expression (eQTL), and protein abundance (pQTL) from respective quantitative trait locus (QTL) studies along with GWAS summary data for nephrolithiasis, ureterolithiasis and bladder calculus from the Million Veteran Program (discovery), with replication in FinnGen and UK Biobank. Summary-data-based Mendelian randomization (SMR) and colocalization were applied to infer causality. Results: Integrated analysis identified Conclusion: This multi-omics MR study links mitochondrial genes, particularly FXN, to urolithiasis risk. Although colocalization evidence was weak (PP.H4 = 0.0239) and replication in independent cohorts was not statistically significant, the multi-omics consistency across methylation, expression, and protein levels prioritizes FXN as a hypothesis-generating candidate for further investigation. Because all QTL data are blood- or plasma-derived, this study provides blood/plasma QTL-based genetic prioritization rather than kidney-specific causal inference.
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.