ArticleScientific reports2025
Analyzing exosomal miRNA profiles in tetralogy of fallot fetuses' amniotic fluid.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Maternal-fetal microRNA axis in congenital heart disease: implications for tetralogy of Fallot.Frontiers in cardiovascular medicine · 2026Review
- The Hidden Regulators: MicroRNAs in Pediatric Heart Development and Disease.Journal of clinical medicine · 2025Review
- Review
- The Role of miRNA Expression in Congenital Heart Disease: Insights into the Mechanisms and Biomarker Potential.Children (Basel, Switzerland) · 2025Review
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Amniotic fluid (AF)-derived exosomal miRNA have been explored as potential contributors to the pathogenesis of Tetralogy of Fallot (TOF). This study aimed to investigate the expression profiles of AF-derived exosomal miRNAs and their potential contribution to TOF development. Exosomes were isolated from AF samples obtained from pregnant women carrying fetuses diagnosed with TOF. AF-derived exosomal miRNAs expression profiles were generated using the Agilent human miRNA Array V21.0, comparing 5 TOF samples with 5 healthy controls. Differential expression analysis identified 257 significantly dysregulated miRNAs in the TOF group. KEGG pathway enrichment analysis revealed that the predicted targets of these differentially expressed miRNAs were enriched in pathways associated with congenital disorders. Notably, 25 of these miRNAs were previously reported to be regulated by both Notch and Wnt signaling pathways, which are critical to heart development. Further investigation using mouse embryonal carcinoma P19 cells revealed that miR-10a-5p overexpression inhibited cardiomyogenic differentiation, as evidenced by the suppression of cardiomyocyte marker genes like TBX5. A dual-luciferase reporter assay confirmed TBX5 as a direct target of miR-10a-5p, suggesting a regulatory mechanism involving their interaction. In summary, our study demonstrates that miR-10a-5p may contribute to the pathogenesis of TOF by impairing cardiomyocyte differentiation through direct targeting of TBX5. These findings enhance our understanding of TOF and its molecular underpinnings.
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