ArticleJournal of the American Heart Association2025
Identification of Long Noncoding RNA Candidate Disease Genes Associated With Clinically Reported Copy Number Variants in Congenital Heart Disease.
Article in Journal of the American Heart Association, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Reannotation of Public Transcriptomic Data Identifies Candidate lncRNAs and Putative Regulatory Networks in Rhabdomyosarcoma.Biomedicines · 2026Article
- Comprehensive analysis of copy number variations in congenital heart defects Tunisian patients: chromosomal microarray analysis insights.Molecular cytogenetics · 2026Article
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Authors and funding
8 authors.
Funding
Abstract
backgroundCopy number variants (CNVs) contribute to 3% to 10% of isolated congenital heart disease (CHD) cases, yet their pathogenic roles remain unclear. Diagnostic efforts have focused on protein-coding genes, largely overlooking long noncoding RNAs (lncRNAs), which play key roles in development and disease. METHODS AND
resultsWe systematically analyzed lncRNAs overlapping clinically validated CNVs in 743 patients with CHD from the Cytogenomics of Cardiovascular Malformations Consortium. We identified heart-expressed lncRNAs, constructed a gene regulatory network using weighted gene coexpression network analysis, and identified gene modules associated with heart development. Functional enrichment and network analyses were used to identify lncRNAs that may be involved in heart development and potentially contribute to CHD. The code is stably archived at https://doi.org/10.5281/zenodo.13799779. We identified 18 lncRNA candidate genes within modules significantly correlated with heart tissue, highlighting their potential involvement in CHD pathogenesis. Notably, lncRNAs such as
conclusionsUsing weighted gene coexpression network analysis, we identified CNV-associated lncRNAs with potential relevance to CHD, underscoring the complexities of noncoding regions in disease pathogenesis. These findings suggest that lncRNAs may play a greater role in CHD than previously recognized, highlighting the need for broader genomic analyses that extend beyond protein-coding genes. This study provides a foundation for further exploration of lncRNAs in CHD, with potential implications for improved genetic characterization and diagnosis.
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