Which mitochondrial genes may drive IBD risk?
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.
Source
Multi-omic insight into the molecular networks of mitochondrial dysfunction in the pathogenesis of inflammatory bowel disease
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
Structured fields used in claim comparison tables when every cited study has a complete layer.
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
What they did
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.
What they found
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.
The limits
What it doesn't show
MR associations are not clinical proof that modulating these proteins treats IBD; horizontal pleiotropy and cohort differences remain risks.
Key terms
- Mendelian randomization
- Uses genetic variants as instruments to infer causal effects.
- Colocalization
- Tests whether two traits share the same causal variant.
- mQTL/eQTL/pQTL
- Loci affecting methylation, expression, or protein levels.
- PARK7
- Mitochondrial-related gene with tier-1 IBD evidence here.
- ACADM
- Fatty-acid oxidation gene linked to UC across omics.
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Tier-1 genes highlighted were:
Common questions
Tier-1 genes?
PARK7 and ACADM.
PARK7 protein OR for IBD?
0.36 (95% CI 0.25–0.52).
Methods?
MR + colocalization across m/e/pQTLs.
Replication GWAS?
UK Biobank and FinnGen.
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