Single-nucleus multi-omics implicates androgen receptor signaling in cardiomyocytes and NR4A1 regulation in fibroblasts during atrial fibrillation DOI Creative Commons
Francis Leblanc, Chi Him Kendrick Yiu, Lucia M. Moreira

и другие.

Nature Cardiovascular Research, Год журнала: 2025, Номер unknown

Опубликована: Март 25, 2025

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 left appendages individuals with AF non-AF controls. We combined a appendage single-nucleus multi-omics dataset to assign specific cell types. found noncoding at IFNG locus LINC01479 , IFNG-AS1 ) strongly dysregulated cardiomyocytes. defined signature potentially driven by androgen receptor signaling cardiomyocytes AF. Cell-type-specific modules suggested an increase T decrease adipocyte neuronal Lastly, showed that reducing NR4A1 expression, marker poorly characterized fibroblast subtype, activation markers, extracellular matrix remodeling proliferation decreased.

Язык: Английский

Single-nucleus multi-omics implicates androgen receptor signaling in cardiomyocytes and NR4A1 regulation in fibroblasts during atrial fibrillation DOI Creative Commons
Francis Leblanc, Chi Him Kendrick Yiu, Lucia M. Moreira

и другие.

Nature Cardiovascular Research, Год журнала: 2025, Номер unknown

Опубликована: Март 25, 2025

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 left appendages individuals with AF non-AF controls. We combined a appendage single-nucleus multi-omics dataset to assign specific cell types. found noncoding at IFNG locus LINC01479 , IFNG-AS1 ) strongly dysregulated cardiomyocytes. defined signature potentially driven by androgen receptor signaling cardiomyocytes AF. Cell-type-specific modules suggested an increase T decrease adipocyte neuronal Lastly, showed that reducing NR4A1 expression, marker poorly characterized fibroblast subtype, activation markers, extracellular matrix remodeling proliferation decreased.

Язык: Английский

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