ArticleJournal of cardiovascular electrophysiology2026
Single-Cell Transcriptomics and Mendelian Randomization Analysis Reveal Key Genes in Atrial Fibrillation.
Article in Journal of cardiovascular electrophysiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
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Who cites it
1 citing paper in PubMed.
- Single-Cell Transcriptomics and Mendelian Randomization Analysis Reveal Key Genes in Atrial Fibrillation.Journal of cardiovascular electrophysiology · 2026Article
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Authors and funding
6 authors.
Funding
Abstract
backgroundAtrial fibrillation (AF) is one of the most common cardiac arrhythmias. It reduces quality of life and increases the risk of complications such as stroke. Although progress has been made in understanding its pathogenesis, the key cellular subtypes and therapeutic targets remain unclear.
methodsWe applied single-cell transcriptomics to identify critical cellular subtypes in AF. High-dimensional weighted gene co-expression network analysis (hdWGCNA) and machine learning were used to screen AF-related genes. Mendelian randomization (MR) and colocalization analyses were performed to assess causal relationships between these genes and AF.
resultsSingle-cell analysis showed a significant increase in macrophages in AF, especially SPP1-expressing macrophages, which may drive AF onset and progression. HdWGCNA identified AF-related gene modules. Three genes, LRCH1, RSRC2 and VAMP2, were found to be causally associated with AF. MR analysis confirmed their significant causal effects.
conclusionsThe accumulation of SPP1-expressing macrophages may drive the onset and progression of AF. Furthermore, LRCH1, RSRC2, and VAMP2 were identified as key causal genes for AF, providing novel insights into its molecular mechanisms and potential therapeutic targets.
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