ArticleCell genomics2024
eQTLs identify regulatory networks and drivers of variation in the individual response to sepsis.
Article in Cell genomics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.
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Who cites it
12 citing papers in PubMed, 1 synthesis or guideline pooled it.
- A consensus blood transcriptomic framework for sepsis.Nature medicine · 2025Guideline
- Deleterious variants in LTBP4 are associated with severe pediatric sepsis.Pediatric research · 2026Article
- Human Genetic Analysis Reveals Circulating Alpha-1 Antitrypsin Level as a Protective Factor in Sepsis.medRxiv : the preprint server for health sciences · 2026Article
- Context-specific regulatory genetic variation in MTOR dampens neutrophil-T cell crosstalk in pneumonia-associated sepsis.Nature communications · 2026Article
- Rare genetic variant risks in patients with sepsis-associated acute respiratory distress syndrome.Respiratory research · 2026Article
- Progenitor CD8Apoptosis : an international journal on programmed cell death · 2026Article
- Genomic and integrative based progression biomarker discovery in adult sepsis: toward clinical stratification and precision medicine.Annals of intensive care · 2026Review
- Pediatric critical illness endotypes reveal distinct outcomes and immune pathways shared across cause of illness.iScience · 2025Article
- The circulating cell-free DNA landscape in sepsis is dominated by impaired liver clearance.Cell genomics · 2025Article
- Population-specific genetic-risk scores enable improved prediction of mortality within 28 days of sepsis onset: a retrospective Taiwanese cohort study.Journal of intensive care · 2025Article
- EQTL analyses are a formidable tool to define the immunogenetic mechanisms underpinning Spondyloarthropathies.Frontiers in immunology · 2025Article
- Sepsis research: Heterogeneity as a foundation rather than an afterthought.Cell genomics · 2024Article
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Authors and funding
14 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sepsis is a clinical syndrome of life-threatening organ dysfunction caused by a dysregulated response to infection, for which disease heterogeneity is a major obstacle to developing targeted treatments. We have previously identified gene-expression-based patient subgroups (sepsis response signatures [SRS]) informative for outcome and underlying pathophysiology. Here, we aimed to investigate the role of genetic variation in determining the host transcriptomic response and to delineate regulatory networks underlying SRS. Using genotyping and RNA-sequencing data on 638 adult sepsis patients, we report 16,049 independent expression (eQTLs) and 32 co-expression module (modQTLs) quantitative trait loci in this disease context. We identified significant interactions between SRS and genotype for 1,578 SNP-gene pairs and combined transcription factor (TF) binding site information (SNP2TFBS) and predicted regulon activity (DoRothEA) to identify candidate upstream regulators. Overall, these approaches identified putative mechanistic links between host genetic variation, cell subtypes, and the individual transcriptomic response to infection.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.