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Updated: May 6, 2026

Electrophysiological Assessment of Murine Atria with High-Resolution Optical Mapping
Published on: February 22, 2018
Gene expression and genetic variation in human atria
Honghuang Lin1, Elena V Dolmatova2, Michael P Morley3
1National Heart Lung and Blood Institute's and Boston University's Framingham Heart Study, Framingham, Massachusetts; Section of Computational Biomedicine, Department of Medicine, Boston University School of Medicine, Boston, Massachusetts.
Researchers identified distinct gene expression patterns in the human left and right atria, revealing MYOZ1 as a potential cause of atrial fibrillation (AF). This study advances understanding of AF molecular mechanisms.
Area of Science:
- Genomics and Molecular Biology
- Cardiovascular Research
- Atrial Fibrillation Pathophysiology
Background:
- Human atria exhibit differential susceptibility to atrial fibrillation (AF).
- Molecular underpinnings of AF-related structural and functional atrial changes remain unclear.
Purpose of the Study:
- To comprehensively characterize gene expression profiles in human left and right atria.
- To identify genetic variations within human atrial tissues.
Main Methods:
- Analysis of 53 left atrial and 52 right atrial tissue samples from the MAGNet repository.
- Gene expression profiling using Affymetrix GeneChip Human Genome U133A Array.
- Genetic variation analysis via Affymetrix Genome-Wide Human SNP Array 6.0.
Main Results:
- 109 genes showed differential expression between left and right atria.
- Significant cis-associations between transcript levels and genetic variants were identified in both atria.
- SNP rs3740293 at a known AF locus associated with MYOZ1 expression in both atria.
Conclusions:
- A distinct transcriptional profile exists between the human right and left atrium.
- Extensive cis-associations link atrial transcripts with common genetic variants.
- MYOZ1 is implicated as the causative gene at the chromosome 10q22 locus for AF.
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