Unraveling the dual role of fibroblast growth factor 5 (FGF5) in cardiorenal diseases through multi-omics causal inference
Authors' conclusion
This study systematically elucidates the potential antagonistic pleiotropic effects of FGF5 across cardiorenal diseases.
Study context
- Population
- Four large-scale protein quantitative trait loci (pQTL) cohorts from European and East Asian populations; 2719 plasma proteins and 34 age-related diseases4 pQTL cohorts
- Outcome
- FGF5 and cardiorenal diseases
Methodological detailsmulti-omics causal inference, dual-window Bayesian colocalization, Mendelian randomization, observational cross-sectional analysis, genetic fine-mapping, cis-regulatory element analysis, single-cell transcriptomics
- Multi-omics causal inference
- Dual-window Bayesian colocalization
- Mendelian randomization
- Observational cross-sectional analysis
- Genetic fine-mapping
- Cis-regulatory element analysis
- Single-cell transcriptomics
Main finding
As reported in the abstract
FGF5 pQTL signals colocalized with expression quantitative trait loci (eQTL) signals exclusively in renal cortex, glomeruli and renal tubules (PP.H4)
> 0.97
Mendelian randomization (MR): genetically predicted higher circulating FGF5 associated with increased CVD risk; proportion potentially mediated by blood pressure
42.9-66.7%
MR: potentially protective effect of higher FGF5 on chronic kidney disease (CKD); proportion potentially mediated by uric acid
8.4-11.8%
Original publication
Unraveling the dual role of fibroblast growth factor 5 (FGF5) in cardiorenal diseases through multi-omics causal inference. Cardiovasc Diabetol. Published 26 July 2026. doi:10.
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