ArticleCurrent medicinal chemistry2025
Bioinformatics-based Analysis and Verification of Chromatin Regulators and the Mechanism of Immune Infiltration Associated with Myocardial Infarction.
Article in Current medicinal chemistry, 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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4 citing papers in PubMed.
- Exploring PANoptosis Related Novel Diagnostic Biomarkers and Potential Drugs for Sarcopenia based on Machine Learning and Experimental Validation.Current medicinal chemistry · 2025Article
- The N-6 methyladenosine dynamics in STEMI and the effect of IL-6 inhibition - a hypothesis generating sub-study of the ASSAIL-MI trial.Frontiers in immunology · 2025Article
- Upregulated haptoglobin in classical monocytes serves as a diagnostic and immunological biomarker in myocardial infarction: a cross-sectional multi-omics study.Frontiers in immunology · 2025Article
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Abstract
backgroundRecent studies have shown that dysfunction in chromatin regulators (CRs) may be an important mechanism of myocardial infarction (MI). They are thus expected to become a new target in the diagnosis and treatment of MI. However, the diagnostic value of CRs in MI and the mechanisms are not clear.
methodsCRs-related differentially expressed genes (DEGs) were screened between healthy controls and patients with MI via GSE48060, GSE60993, and GSE66360 datasets. DEGs were further analyzed for enrichment analysis. Hub genes were screened by least absolute shrinkage and selection operator (LASSO) regression and weighted gene co-expression network analysis (WGCNA). GSE61144 datasets were further used to validate hub genes. RT-qPCR examined peripheral blood mononuclear cells (PBMCs) to verify expressions of hub genes. In addition, a correlation between hub genes and immune cell infiltration was identified by CIBERSORT and single-sample gene set enrichment analysis (ssGSEA). Finally, we constructed a diagnostic nomogram and ceRNA network and found possible therapeutic medicines which were based on hub genes.
resultsFirstly, 16 CR-related DEGs were identified. Next, Dual-specificity phosphatase 1 (<i>DUSP1</i>), growth arrest and DNA damage-inducible 45 (GADD45A), and transcriptional regulator Jun dimerization protein 2 (<i>JDP2</i>) were selected as hub genes by LASSO and WGCNA. Receiver operating characteristic curves in the training and test data sets verified the reliability of hub genes. Results of RT-qPCR confirmed the upregulation of hub genes in MI. Subsequently, the immune infiltration analysis indicated that <i>DUSP1</i>, GADD45A</i>, and <i>JDP2</i> were correlated with plasmacytoid dendritic cells, natural killer cells, eosinophils, effector memory CD4 T cells, central memory CD4 T cells, activated dendritic cells, and activated CD8 T cells. Furthermore, a nomogram that included <i>DUSP1</i>, GADD45A</i>, and <i>JDP2</i> was created. The calibration curve, decision curve analysis, and the clinical impact curve indicated that the nomogram could predict the occurrence of MI with high efficacy. The results of the ceRNA network suggest that hub genes may be cross-regulated by various lncRNAs and miRNAs. In addition, 10 drugs, including 2H-1-benzopyran, Nifuroxazide, and Bepridil, were predicted to be potential therapeutic agents for MI.
conclusionOur study identifies three promising genes associated with the progression of chromatin regulators (CRs)-related myocardial infarction (MI) and immune cell infiltration, including Dual-specificity phosphatase 1 (
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