ArticleNature cardiovascular research2025
Single-nucleus multi-omics implicates androgen receptor signaling in cardiomyocytes and NR4A1 regulation in fibroblasts during atrial fibrillation.
Article in Nature cardiovascular research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Reversing the pipeline: a 'human-first' multi-omics approach to cardiovascular discovery.Experimental & molecular medicine · 2026Review
- Protocol for isolation of nuclei from murine cardiac tissue for single-nucleus multiomic sequencing.STAR protocols · 2026Article
- Cardiac fibroblasts in myocardial injury and heart failure.European heart journal · 2026Review
- Cardiac Macrophages and Fibroblasts Modulate Atrial Fibrillation Maintenance.Circulation research · 2026Article
- Autofluorescence and deep learning in early disease detection: biological foundations, clinical applications, and future directions.Frontiers in artificial intelligence · 2026Review
- Single-cell multi-omics for precision cardiovascular and longevity medicine: from methods to clinical translation.Frontiers in aging · 2025Review
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Authors and funding
10 authors.
Funding
Abstract
The dysregulation of gene expression programs in the human atria during persistent atrial fibrillation (AF) is not completely understood. Here, we reanalyze bulk RNA-sequencing datasets from two studies (N = 242) and identified 755 differentially expressed genes in left atrial appendages of individuals with persistent AF and non-AF controls. We combined the bulk RNA-sequencing differentially expressed genes with a left atrial appendage single-nucleus multi-omics dataset to assign genes to specific atrial cell types. We found noncoding genes at the IFNG locus (LINC01479, IFNG-AS1) strongly dysregulated in cardiomyocytes. We defined a gene expression signature potentially driven by androgen receptor signaling in cardiomyocytes from individuals with AF. Cell-type-specific gene expression modules suggested an increase in T cell and a decrease in adipocyte and neuronal cell gene expression in AF. Lastly, we showed that reducing NR4A1 expression, a marker of a poorly characterized human atrial fibroblast subtype, fibroblast activation markers, extracellular matrix remodeling and cell proliferation decreased.
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