Screening and Bioinformatics Analysis of Differentially Expressed miRNAs in Pediatric Fulminant Myocarditis

DOI: 10.12201/bmr.202503.00064

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  Abstract: Abstract Objective To analyze the differentially expressed miRNAs and their target genes in the serum of pediatric patients with fulminant myocarditis through bioinformatics methods, and to explore the pathogenesis. Methods We selected the GSE221090 dataset from the Gene Expression Omnibus (GEO) high-throughput gene expression database, and bio-informatics analysis was performed using the GEO2R online tool to screen for differentially expressed miRNAs. The online miRDB database was used to predict the target genes of the differentially expressed miRNAs. The DAVID tool was employed for GO enrichment analysis and KEGG pathway analysis of the screened target genes. Additionally, a protein-protein interaction network (PPI) associated with the differentially expressed genes was constructed using the STRING database and Cytoscape software, and core genes were screened. Results A total of 148 differentially expressed miRNAs were identified in the serum of the pediatric fulminant myocarditis group compared to a control group of normal children,including 109 up-regulated and 39 down-regulated miRNAs. We selected the top ten up-regulated and down-regulated miRNAs based on their scores, and target gene prediction for the aforementioned miRNAs was conducted using the online miRDB database, identifying 291 target genes regulated by up-regulted miRNAs and 290 target genes regulated by down-regulated miRNAs. Subsequent GO and KEGG analyses demonstrated that the target genes of up-regulated miRNAs were primarily enriched in signaling pathways including PI3K-Akt and FoxO, whereas the target genes of down-regulated miRNAs predominantly participated in the TGF-β signaling pathway and related pathways. We identified the top ten differentially expressed genes with the highest relevance scores using PPI and Cytoscape software, including SIRT1, STAT3, ESR1, H3-3B, NCOR1, IRF4, IL1B, DICER1, HDAC1, and DDX6. Conclusion MiR-22-3p, miR-4284, and others are crucial in the pathogenesis of pediatric fulminant myocarditis, possibly related to the expression levels of SIRT1 and HDAC1 they regulate, with mechanisms that may exert biological effects via the PI3K-Akt, TGF-β, and other signaling pathways.

  Key words: Fulminant myocarditis; Gene chip; Bioinformatics

  Submit time: 21 March 2025

  Copyright: The copyright holder for this preprint is the author/funder, who has granted biomedRxiv a license to display the preprint in perpetuity.
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