ArticleCell reports2023
Tissue-specific and tissue-agnostic effects of genome sequence variation modulating blood pressure.
Article in Cell reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed, 8 citations in OpenAlex.
- Partitioned blood pressure polygenic risk reveals differential genetic effects of tissue-specific enhancers and their interactions on cardiovascular disease.Research square · 2026Article
- Controversy in Hypertension: Pro-Side of the Argument Using Artificial Intelligence for Hypertension Diagnosis and Management.Hypertension (Dallas, Tex. : 1979) · 2025Review
- Machine learning and multi-omics integration: advancing cardiovascular translational research and clinical practice.Journal of translational medicine · 2025Review
- Chromatin State Maps of Blood Pressure-Relevant Renal Segments Reveal Potential Regulatory Role for SNPs.Hypertension (Dallas, Tex. : 1979) · 2025Article
- Identification of the Molecular Components of Enhancer-Mediated Gene Expression Variation in Multiple Tissues Regulating Blood Pressure.Hypertension (Dallas, Tex. : 1979) · 2024Article
- Sex-specific genetic architecture of blood pressure.Nature medicine · 2024Article
- Mapping genomic regulation of kidney disease and traits through high-resolution and interpretable eQTLs.Nature communications · 2023Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Genome-wide association studies (GWASs) have identified numerous variants associated with polygenic traits and diseases. However, with few exceptions, a mechanistic understanding of which variants affect which genes in which tissues to modulate trait variation is lacking. Here, we present genomic analyses to explain trait heritability of blood pressure (BP) through the genetics of transcriptional regulation using GWASs, multiomics data from different tissues, and machine learning approaches. Approximately 500,000 predicted regulatory variants across four tissues explain 33.4% of variant heritability: 2.5%, 5.3%, 7.7%, and 11.8% for kidney-, adrenal-, heart-, and artery-specific variants, respectively. Variation in the enhancers involved shows greater tissue specificity than in the genes they regulate, suggesting that gene regulatory networks perturbed by enhancer variants in a tissue relevant to a phenotype are the major source of interindividual variation in BP. Thus, our study provides an approach to scan human tissue and cell types for their physiological contribution to any trait.
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