genetics
Which mitochondrial genes may drive IBD risk?
Open access · cc by · source: Europe PMC
Integrating methylation, expression, and protein QTLs via MR/colocalization flags PARK7 and ACADM as tier-1 mitochondrial genes for IBD/UC, with protective protein-level odds ratios.
How this study connects
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Study at a glance
- Design
- Computational / modelling — Multi-omics Mendelian randomization + colocalization of mitochondrial QTLs vs IBD
- N
- N=2 · Two tier-1 mitochondrial genes (PARK7, ACADM); discovery IBDGC with UKB/FinnGen replication
- Population
- Genetic instruments from mQTL/eQTL/pQTL studies vs IBD/UC/CD GWAS
- Outcome
- Putative causal mitochondrial gene–IBD associations across omics layers
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Inspect source passages
Which mitochondrial genes may drive IBD risk?
These passages occur verbatim in the stored paper text. They support the points listed below; they do not verify every statement in the explanation.
Higher PARK7 protein linked to lower IBD risk (OR 0.36).
genetically predicted higher levels of PARK7 (OR 0.36, 95% CI 0.25–0.52)
HINT1 OR 0.47 for IBD; OR 0.26 for CD.
HINT1 (OR 0.47, 95% CI 0.30–0.74) were inversely associated with IBD risk
Key findings
PARK7 and ACADM had tier-1 multi-omic support for IBD/UC; PDK1 and FIS1 had weaker UC tiers. Higher genetically predicted PARK7 (OR 0.36) and HINT1 (OR 0.47) associated with lower IBD risk; higher HINT1 with lower CD (OR 0.26); higher ACADM/PDK1/FIS1 with lower UC.
Methodology
Used summary-data MR on mitochondrial gene methylation, expression, and protein QTLs against IBDGC (discovery) plus UK Biobank and FinnGen (replication), with colocalization to test shared causal variants.
Limitations
MR associations are not clinical proof that modulating these proteins treats IBD; horizontal pleiotropy and cohort differences remain risks.
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