Trial reportPloS one2014
Genome-wide identification of expression quantitative trait loci (eQTLs) in human heart.
Trial report in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 4 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
33 citing papers in PubMed, 4 syntheses or guidelines pooled it, 47 citations in OpenAlex.
- Large-scale pharmacogenomic study of sulfonylureas and the QT, JT and QRS intervals: CHARGE Pharmacogenomics Working Group.The pharmacogenomics journal · 2018Pooled it
- A Genomewide Integrative Analysis of GWAS and eQTLs Data Identifies Multiple Genes and Gene Sets Associated with Obesity.BioMed research international · 2018Pooled it
- Pooled it
- The genetics of blood pressure regulation and its target organs from association studies in 342,415 individuals.Nature genetics · 2016Pooled it
- Integration of dilated cardiomyopathy genomics with transcriptomics from the human heart implicates regulatory molecular mechanisms.medRxiv : the preprint server for health sciences · 2026Article
- CD73 polymorphisms are associated with schizophrenia.Purinergic signalling · 2025Article
- Article
- Personalized transcriptome signatures in a cardiomyopathy stem cell biobank.bioRxiv : the preprint server for biology · 2024Article
- Phenotypic but not genetically predicted heart rate variability associated with all-cause mortality.Communications biology · 2023Article
- Article
- The Genetics and Epigenetics of Ventricular Arrhythmias in Patients Without Structural Heart Disease.Frontiers in cardiovascular medicine · 2022Review
- Mending a broken heart:Disease models & mechanisms · 2021Review
- Dynamic effects of genetic variation on gene expression revealed following hypoxic stress in cardiomyocytes.eLife · 2021Article
- Disruptive Selection of Human Immunostimulatory and Immunosuppressive Genes Both Provokes and Prevents Rheumatoid Arthritis, Respectively, as a Self-Domestication Syndrome.Frontiers in genetics · 2021Article
- Nongenic cancer-risk SNPs affect oncogenes, tumour-suppressor genes, and immune function.British journal of cancer · 2020Article
- N-myc and STAT interactor correlates with severity and prognosis in acute-on-chronic liver failure of hepatitis B virus.Journal of gastroenterology and hepatology · 2019Article
- Genomic approaches for the elucidation of genes and gene networks underlying cardiovascular traits.Biophysical reviews · 2018Review
- SCN5A: the greatest HITS collection.The Journal of clinical investigation · 2018Article
- A common variant alters SCN5A-miR-24 interaction and associates with heart failure mortality.The Journal of clinical investigation · 2018Article
- Genetic Reduction in Left Ventricular Protein Kinase C-α and Adverse Ventricular Remodeling in Human Subjects.Circulation. Genomic and precision medicine · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 6 institutions in 4 countries.
Funding
Abstract
In recent years genome-wide association studies (GWAS) have uncovered numerous chromosomal loci associated with various electrocardiographic traits and cardiac arrhythmia predisposition. A considerable fraction of these loci lie within inter-genic regions. The underlying trait-associated variants likely reside in regulatory regions and exert their effect by modulating gene expression. Hence, the key to unraveling the molecular mechanisms underlying these cardiac traits is to interrogate variants for association with differential transcript abundance by expression quantitative trait locus (eQTL) analysis. In this study we conducted an eQTL analysis of human heart. For a total of 129 left ventricular samples that were collected from non-diseased human donor hearts, genome-wide transcript abundance and genotyping was determined using microarrays. Each of the 18,402 transcripts and 897,683 SNP genotypes that remained after pre-processing and stringent quality control were tested for eQTL effects. We identified 771 eQTLs, regulating 429 unique transcripts. Overlaying these eQTLs with cardiac GWAS loci identified novel candidates for studies aimed at elucidating the functional and transcriptional impact of these loci. Thus, this work provides for the first time a comprehensive eQTL map of human heart: a powerful and unique resource that enables systems genetics approaches for the study of cardiac traits.
Indexed as
Identifiers
What OpenQuestion holds
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.