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Updated: Jul 1, 2025
Estimating Bilateral Atrial Function by Cardiovascular Magnetic Resonance Feature Tracking in Patients with Paroxysmal Atrial Fibrillation
Published on: July 20, 2022
Upregulated Genes in Atrial Fibrillation Blood and the Left Atrium
Takahiro Kamihara1, Tomoyasu Kinoshita2, Reo Kawano2
1Department of Cardiology, National Center for Geriatrics and Gerontology, Obu, Japan.
Insights
This study identified 12 upregulated genes in atrial fibrillation (AF) patients, with lysosome-related genes like FTL and ASAH1 showing particular promise as biomarkers for AF pathogenesis.
Area of Science:
- Cardiology
- Genetics
- Biomarker Discovery
Background:
- Atrial fibrillation (AF) is a common arrhythmia linked to aging, but unexplained cases suggest additional contributing factors.
- Identifying novel biomarkers is crucial for predicting AF risk and complications, especially in aging populations.
Purpose of the Study:
- To identify upregulated genes in peripheral blood and left atrium of patients with AF.
- To explore the potential of these genes as biomarkers for AF onset and complications.
Main Methods:
- Analysis of gene expression data from blood and left atrial samples of AF and sinus rhythm patients.
- Utilized GeneMANIA and Cytoscape for gene function and pathway analysis.
- Employed RefEx to assess tissue-specific gene expression and heatmaps for blood expression levels.
Main Results:
- Identified 12 upregulated genes (e.g., CAST, ASAH1, MAFB, FTL) in both blood and left atrium of AF patients.
- Genes are involved in lysosomal function and lipid metabolism pathways.
- FTL, ASAH1, S100A6, and PABPC1 showed high expression in normal heart tissue, with FTL and ASAH1 implicated in AF pathogenesis.
Conclusions:
- Lysosome-related genes, particularly FTL and ASAH1, play a significant role in AF pathophysiology.
- These genes represent potential targets for future AF research and therapeutic strategies.
Introduction:
Atrial fibrillation (AF) is a common arrhythmia associated with aging. Many known risk factors are associated with AF, but many senior individuals do not develop AF despite having multiple risk factors. This finding suggests that other factors may be involved in AF onset. This study aimed to identify upregulated genes in the peripheral blood and left atrium of patients with AF. These genes may serve as potential biomarkers to predict AF onset risk and its complications.
Methods:
Gene expression data were analyzed from blood (n = 3) and left atrial samples (n = 15) of patients with AF and sinus rhythm. We evaluated the significant genes identified using p value analysis of weighted average difference to confirm their rankings. We created figures for the genes using GeneMANIA and performed a functional analysis using Cytoscape3.10.1. Hub and bottleneck genes were identified based on degree and betweenness centrality. We used reference expression (RefEx) to confirm the organs in which the extracted genes were expressed. Heatmaps and Gene ontology term evaluation were performed to further elucidate the biological functions of the genes.
Results:
We identified 12 upregulated genes (CAST, ASAH1, MAFB, VCAN, DDIT4, FTL, HEXB, PROS1, BNIP3L, PABPC1, YBX3, and S100A6) in both the blood and left atrium of patients with AF. We analyzed the gene functions using GeneMANIA and Cytoscape. The identified genes were involved in a variety of pathways, including lysosomal function and lipid and sphingolipid catabolism. Next, we investigated whether the 12 identified genes identified were systemically expressed or had high organ specificity. Finally, RefEx was used to analyze the gene expression levels in various tissues. Four genes, FTL, ASAH1, S100A6, and PABPC1, were highly expressed in the normal heart tissue. Finally, we evaluated the expression levels of the 12 genes in the blood of patients with AF using a heatmap. Our findings suggest that the 12 genes identified in this study, especially the lysosome-related genes (FTL and ASAH1), may be involved in AF pathogenesis.
Conclusion:
Lysosome-related genes may be important to understand the AF pathophysiology and to develop AF-related future studies.
