ArticleCurrent genomics2025
Integrated Multi-omics Analysis of Hub Genes and miRNA Interactions in Hypertrophic Cardiomyopathy.
Article in Current genomics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Hypertrophic Cardiomyopathy (HCM) is a complex cardiac disorder marked by the thickening of the heart muscle. Methods: HCM and normal control cell lines were cultured in DMEM with 12.5% FBS and 1% penicillin-streptomycin at 37°C and 5% CO Results: To identify DEGs and hub genes implicated in HCM, we analyzed three Gene Expression Omnibus (GEO) datasets (GSE32453, GSE53404, and GSE1134439), extracting the top 1000 DEGs. Venn analysis revealed 21 common down-regulated genes. PPI analysis identified these six as key hub genes, including Iron Response Element Binding Protein 2 (IREB2), Protein Tyrosine Phosphatase, Non-Receptor Type 11 (PTPN11), IQ Motif Containing GTPase Activating Protein 1 (IQGAP1), Phosphoglucomutase 2 (PGM2), DIS3 RNA Exonuclease 3' to 5' (DIS3), Glutamine-Fructose-6-Phosphate Transaminase 1 (GFPT1) in HCM patients. Gene enrichment analysis highlighted the involvement of these genes in cellular functions such as energy metabolism and growth factor signaling, suggesting their role in the disease's progression. Validation using an additional dataset (GSE36961) confirmed significant down-regulation of all hub genes in HCM samples, supported by Receiver Operating Characteristic (ROC) curve analysis that demonstrated their diagnostic potential. Furthermore, miRNA analysis identified six up-regulated miRNAs (miR-124, miR-29b, miR-330, miR-34a, miR-375, and miR-451) that likely contribute to the dysregulation of these hub genes. Drug prediction analysis identified various potential therapeutic compounds targeting these hub genes. Molecular docking revealed favorable binding affinities, supporting the therapeutic potential of these drugs in modulating hub gene activity. Discussion: These findings demonstrate that HCM progression involves coordinated downregulation of hub genes and miRNA-mediated dysregulation of metabolic and signaling pathways. The integration of bioinformatics, validation assays, and drug docking suggests a strong translational potential for biomarker discovery and targeted therapy. Conclusion: Our findings suggest that IREB2, PTPN11, IQGAP1, PGM2, DIS3, and GFPT1 hub genes and their associated regulatory pathways may serve as biomarkers and therapeutic targets for HCM, potentially improving diagnosis and treatment strategies.
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