ArticleShock (Augusta, Ga.)2026
Novel Susceptibility Genes for Sepsis Revealed by a Cross-Tissue Transcriptome-Wide Association Study.
Article in Shock (Augusta, Ga.), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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.
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Who cites it
1 citing paper in PubMed.
- Genome-wide association study of paediatric bacteraemia and sepsis.EBioMedicine · 2026Article
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSepsis, a life-threatening syndrome triggered by a dysregulated host response to infection, continues to impose a substantial global health burden. Advances in genomics and transcriptomics now enable systematic exploration of sepsis pathogenesis at the genetic level. The integration of genome-wide association studies and transcriptome-wide association studies (TWAS) offers a powerful framework to identify causal genetic variants and delineate molecular mechanisms underlying sepsis susceptibility and clinical outcomes.
methodsA cross-tissue TWAS was implemented using UTMOST to integrate sepsis genome-wide association studies summary statistics with transcriptomic data from the Genotype-Tissue Expression version 8 (GTEx v8) project. Candidate genes were validated through complementary approaches: FUSION, FOCUS, and MAGMA. Tissue-specific and pathway enrichment analyses were applied to prioritize sepsis-associated genes and characterize their functional roles in disease-relevant biological processes. Bayesian colocalization and two-sample Mendelian randomization (MR) analyses were employed to infer putative causal relationships between prioritized genes and sepsis risk.
resultsFour genes-ZCCHC4, PDGFB, C18orf54, and ATG4B-demonstrated significant associations with sepsis susceptibility in cross-tissue analyses. Two-sample MR provided evidence for causal effects of genetically regulated expression of these genes on sepsis risk. Bayesian colocalization identified shared causal variants between sepsis-associated loci and expression quantitative trait loci (eQTLs), implicating dysregulation of inflammatory and autophagy pathways in sepsis pathogenesis.
conclusionsOur results highlight the efficacy of cross-tissue TWAS in mapping sepsis-associated loci and elucidating the genetic architecture underlying sepsis susceptibility. These prioritized loci constitute compelling targets for functional validation and represent actionable candidates for therapeutic intervention in sepsis.
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