DUAL ARRHYTHMOGENIC MECHANISMS IN ARRHYTHMOGENIC RIGHT VENTRICULAR CARDIOMYOPATHY: INSIGHTS FROM TRANSCRIPTOMIC PROFILING

Clicks: 20
ID: 331400
2026
Free PDF
Article Quality & Performance Metrics
Overall Quality
Not rated
Combines reader engagement with the AI quality analysis. This article has not been analysed, so there is no overall score — reader engagement is measured and shown alongside.
AI Quality Assessment
Not analyzed
Readership in this journal
Emerging

Ranked #95 of 330 articles by views in European heart journal supplements : journal of the European Society of Cardiology

Most read Least read

Bar heights use a square-root scale. Only the 120 most-read articles are drawn; the journal has 330 in total.

Mint this article as an NFT
Not yet minted

Create a permanent, verifiable on-chain record of this article on the Scimatic Network. The NFT is held in your Journament account, and you can withdraw it to your own wallet at any time.

5 SUSD one-off · no wallet required
Sign in to mint
Abstract
Abstract Background and Aims Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC) is an inherited and progressive disease associated with ventricular arrhythmias (VAs) and sudden cardiac death in young individuals. While fibrofatty replacement is a hallmark feature, the molecular mechanisms linking structural remodelling and cellular dysfunction remain incompletely defined. This study aimed to characterise transcriptomic alterations and identify key pathways contributing to arrhythmogenesis in ARVC. Methods Publicly available RNA-seq datasets of right ventricular tissue (GSE107475 for ARVC; GSE107156 for controls) and induced pluripotent stem cell-derived cardiomyocytes (GSE115621) for validation were analysed. Differential expression analysis was performed using limma (adjusted p-values < 0.05). Principal component analysis and hierarchical clustering assessed sample variability and group separation. Functional enrichment analyses were conducted using Gene Ontology and KEGG pathways. Protein-protein interaction (PPI) networks were constructed via STRING to identify key hub genes. Results A total of 1,442 differentially expressed genes were identified from 25,367 analysed transcripts. Principal component analysis demonstrated heterogeneity among ARVC samples, with partial separation from controls. Enrichment analyses revealed significant upregulation of pathways related to extracellular matrix (ECM) organisation, mitochondrial metabolism, oxidative phosphorylation, and oxidative stress responses. PPI network analysis highlighted key hub genes, including COL1A1, GREM1, WNT9A, SOX2, HSPA2, and GDNF, suggesting interconnected networks linking fibrotic remodeling and metabolic stress pathways. Conclusion ARVC exhibits a dual arrhythmogenic mechanism characterised by ECM remodelling facilitating reentry and metabolic dysregulation promoting triggered activity. These findings provide mechanistic insight and highlight potential molecular targets for arrhythmia risk stratification and therapeutic development.
Reference Key
openalex_W7220459251 Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors M Kause, S Zhang
Journal European heart journal supplements : journal of the European Society of Cardiology
Year 2026
DOI
10.1093/eurheartjsupp/suag119.004
URL
https://doi.org/10.1093/eurheartjsupp/suag119.004
Keywords Keywords not found

Citations

No citations found. To add a citation, contact the admin at info@scimatic.org

Comments

No comments yet. Be the first to comment on this article.