ArticlePLoS computational biology2026
Systematic prioritization of potential therapeutic targets for glomerulonephritis using multi-omics Mendelian randomization.
Article in PLoS computational biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Per- and polyfluoroalkyl substances and kidney disease: Genetic associations and computational prioritization of candidate toxicogenomic pathways.PLoS computational biology · 2026Article
- Multi-omics and genetic prioritization identify candidate molecular links between micro- and nanoplastics-associated signatures and chronic kidney disease.Molecular diversity · 2026Article
- Cell type-stratified immunogenetic framework reveals immune drivers and therapeutic targets in kidney stone disease.Molecular therapy. Nucleic acids · 2026Article
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glomerulonephritis (GN) is an immune-mediated kidney disorder that causes glomerular injury, progressive renal dysfunction, and end-stage kidney disease. Traditional treatments such as corticosteroids and immunosuppressants are limited by variable efficacy and severe adverse effects, highlighting the need for novel therapeutic targets and personalized strategies. We performed a systematic multi-omics Mendelian randomization (MR) analysis applying established proteomic and transcriptomic quantitative trait loci (pQTL/eQTL) resources to genome-wide association studies (GWAS) of four GN subtypes: acute, chronic, IgA nephropathy, and membranous nephropathy. Bayesian colocalization was used to strengthen causal inference, while independent replication and meta-analysis were conducted using the FinnGen cohort. Mouse knockout phenotypes, drug reposition, and computational pharmacology algorithm were applied to evaluate translational potential. Proteomic-wide MR revealed MTR as protective in chronic GN and HCK as a risk factor for membranous nephropathy, whereas CD302 and CDKN1B showed protective effects. Transcriptomic-wide MR identified candidate genes across GN subtypes: RECQL, BRSK2, and MGP in acute GN; AFM, CFHR5, and EPHB2 in chronic GN; IL6R, MBL2, and PRSS3 in IgA nephropathy; and TIMP4, HCK, and PEAR1 in membranous nephropathy. Bayesian colocalization analysis provided strong support for shared causal variants (PPH4 > 0.8) for HCK, CD302, TIMP4, PEAR1, PARP1, and FHIT. Replication and meta-analysis in the FinnGen cohort provided additional consistency across datasets, while downstream translational annotations highlighted IL6R, MBL2, C5, and CD55 as potential hub targets within immune and complement-related pathways. This integrative multi-omics study provides novel insights into the genetic architecture and therapeutic landscape of GN, identifying potential therapeutic targets that may inform precision nephrology and drug repurposing. Notably, most targets supported by colocalization, mouse knockout phenotypes, and drug repurposing evidence were predominantly identified in membranous nephropathy, suggesting a particularly tractable genetic and therapeutic architecture for this subtype.
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