ArticleNature communications2019
Mendelian randomization integrating GWAS and eQTL data reveals genetic determinants of complex and clinical traits.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 214 papers, 5 of them syntheses that pooled it.
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.
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Who cites it
214 citing papers in PubMed, 5 syntheses or guidelines pooled it.
- Association between frailty and depression: A bidirectional Mendelian randomization study.Science advances · 2023Pooled it
- Transcriptomic risk scores for attention deficit/hyperactivity disorder.Molecular psychiatry · 2023Pooled it
- Mendelian randomization uncovers a protective effect of interleukin-1 receptor antagonist on kidney function.Communications biology · 2023Pooled it
- Establishing gene regulatory networks from Parkinson's disease risk loci.Brain : a journal of neurology · 2022Pooled it
- Genome-wide Association Study Identified Chromosome 8 Locus Associated with Medication-Related Osteonecrosis of the Jaw.Clinical pharmacology and therapeutics · 2021Pooled it
- GLG1 in cancer-associated fibroblasts promotes bladder cancer growth while limiting tumor apoptosis.Apoptosis : an international journal on programmed cell death · 2026Article
- Cell-type-specific genetic architecture reveals neuronal and immune contributions to neuropsychiatric disorders.Molecular psychiatry · 2026Article
- Two-sample Mendelian randomization study of gut microbiota and inflammatory proteins: Predictive, preventive, and personalized treatment for migraine.Neural regeneration research · 2026Article
- Identification and Validation of Key Genes Related to Arginine Methylation Modification in Sepsis Using Transcriptome Combined with Mendelian Randomization Analysis.Shock (Augusta, Ga.) · 2026Article
- Integrating immune-cell transcriptomic data with Mendelian randomisation reveals novel causal genes for type 2 diabetes and its complications.Diabetologia · 2026Article
- Migraine immune cell gene targets and their relationship to psychiatric disorders.The journal of headache and pain · 2026Article
- CIT-Lasso: a scalable approach beyond guilty by association for identifying causal variants from genome-wide summary statistics.Genome biology · 2026Article
- Computational strategies for copy number variation detection, disease association, and beyond.Genome biology · 2026Review
- Integrated multi-omics analysis reveals key molecular mechanisms underlying fibroproliferation and immune dysregulation in keloids.Functional & integrative genomics · 2026Article
- Integration of genetic evidence to identify approved drug targets.Genome medicine · 2026Article
- Immune cell-specific genetic architecture of Alzheimer's disease revealed by multi-omics analysis for therapeutic target discovery and prioritization.Translational psychiatry · 2026Article
- Genetic and transcriptomic signatures of host control in HIV-1 infection.Retrovirology · 2026Article
- Identification of macrophage polarization-related genes for esophageal cancer risk: a multi-omics Mendelian randomization analysis.Clinical epigenetics · 2026Article
- Deciphering cell type-specific causal genetic effects on brain imaging-derived phenotypes and disorders with single-cell Mendelian randomization.PLoS computational biology · 2026Article
- snRNA-seq identifies Fmo2npj metabolic health and disease · 2026Article
154 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Genome-wide association studies (GWAS) have identified thousands of variants associated with complex traits, but their biological interpretation often remains unclear. Most of these variants overlap with expression QTLs, indicating their potential involvement in regulation of gene expression. Here, we propose a transcriptome-wide summary statistics-based Mendelian Randomization approach (TWMR) that uses multiple SNPs as instruments and multiple gene expression traits as exposures, simultaneously. Applied to 43 human phenotypes, it uncovers 3,913 putatively causal gene-trait associations, 36% of which have no genome-wide significant SNP nearby in previous GWAS. Using independent association summary statistics, we find that the majority of these loci were missed by GWAS due to power issues. Noteworthy among these links is educational attainment-associated BSCL2, known to carry mutations leading to a Mendelian form of encephalopathy. We also find pleiotropic causal effects suggestive of mechanistic connections. TWMR better accounts for pleiotropy and has the potential to identify biological mechanisms underlying complex traits.
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