SynthesisNature communications2023
Genome-wide association analysis and Mendelian randomization proteomics identify drug targets for heart failure.
Synthesis in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers, 6 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.
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
86 citing papers in PubMed, 6 syntheses or guidelines pooled it, 112 citations in OpenAlex.
- Integration of GWAS and single-cell analysis for psoriasis identifies disease-associated cell subtypes and therapeutic targets.Nature communications · 2026Pooled it
- Multi-ancestry genetic architecture of heart failure subtypes.Nature communications · 2026Pooled it
- Genomic data-driven framework for drug target discovery in atrial fibrillation.Journal of translational medicine · 2025Pooled it
- Genome-wide analysis identifies susceptibility loci for heart failure and nonischemic cardiomyopathy subtype in the East Asian populations.PLoS genetics · 2025Pooled it
- Pan-UK Biobank genome-wide association analyses enhance discovery and resolution of ancestry-enriched effects.Nature genetics · 2025Pooled it
- Genetic insights into cardiac conduction disorders from genome-wide association studies.Human genomics · 2025Pooled it
- Integrating multi-omics and mendelian randomization identifies therapeutic targets for Lichen Sclerosus: A druggable genome-wide study.Global medical genetics · 2026Article
- Integrative genomic and proteomic analyses identify candidate genetic loci and genetically supported proteins in age-related macular degeneration.Eye and vision (London, England) · 2026Article
- Advancing PCOS drug development: multi-omics discovery of key targets and repurposable compounds.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Systematic Identification of Therapeutic Targets and Repurposed Drugs for Stroke: From Genome Causal Analysis to Multilevel Validation.Journal of the American Heart Association · 2026Article
- Multi-Omic Insight Into the Molecular Networks of Mitochondrial Dysfunction in the Pathogenesis of Schizophrenia.Schizophrenia bulletin · 2026Article
- LocusPackRat: an R package to support prioritizing candidate genes from large GWAS intervals with standardized evidence aggregation.G3 (Bethesda, Md.) · 2026Article
- Integrative omics analysis incorporating cardiovascular magnetic resonance imaging pinpoints potentially druggable plasma proteins for cardiovascular diseases.Life metabolism · 2026Article
- Molecular Mechanisms and Multi-Omics Integration in Heart Failure: From Pathophysiology to Precision Medicine.International journal of molecular sciences · 2026Review
- Microvascular endothelial scavenger receptor class B type I protects against heart failure with preserved ejection fraction by inhibiting T-cell cardiotropism.EMBO molecular medicine · 2026Article
- Decoding the Heart Failure Peptidome.Circulation. Heart failure · 2026Article
- Methods for Prioritizing Causal Genes in Molecular Studies of Human Disease: The State of the Art.Genetic epidemiology · 2026Review
- Rare coding and noncoding variants map 1,342 diseases and biomarkers in 490,549 whole genomes.medRxiv : the preprint server for health sciences · 2026Article
- Integrative mendelian randomization approaches for therapeutic target prioritisation in immune-mediated diseases.Scientific reports · 2026Article
- Genome-wide analysis of cardiac ventricular phenotypes reveals novel loci and therapeutic targets for heart failure.Nature communications · 2026Article
26 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
35 authors at 16 institutions in 5 countries.
Funding
Abstract
We conduct a large-scale meta-analysis of heart failure genome-wide association studies (GWAS) consisting of over 90,000 heart failure cases and more than 1 million control individuals of European ancestry to uncover novel genetic determinants for heart failure. Using the GWAS results and blood protein quantitative loci, we perform Mendelian randomization and colocalization analyses on human proteins to provide putative causal evidence for the role of druggable proteins in the genesis of heart failure. We identify 39 genome-wide significant heart failure risk variants, of which 18 are previously unreported. Using a combination of Mendelian randomization proteomics and genetic cis-only colocalization analyses, we identify 10 additional putatively causal genes for heart failure. Findings from GWAS and Mendelian randomization-proteomics identify seven (CAMK2D, PRKD1, PRKD3, MAPK3, TNFSF12, APOC3 and NAE1) proteins as potential targets for interventions to be used in primary prevention of heart failure.
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Registered trials
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 OpenQuestion graph.