ArticleJournal of inflammation research2024
Role of Cellular Senescence Genes and Immune Infiltration in Sepsis and Sepsis-Induced ARDS Based on Bioinformatics Analysis.
Article in Journal of inflammation research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Machine learning methods identified cellular senescence-related hub molecules in sepsis-induced acute respiratory distress syndrome (ARDS) and their upstream regulatory network.Molecular biology reports · 2026Article
- Akt/mTOR pathway-mediated CCNA1 regulation of radiotherapy resistance in nasopharyngeal carcinoma.Cellular oncology (Dordrecht, Netherlands) · 2026Article
- Evaluating the Diagnostic Value and Molecular Mechanism of Energy Metabolism-Related Gene PEA15 in Sepsis.Journal of inflammation research · 2026Article
- Combination of machine learning and protein‑protein interaction network established one ATM‑DPP4‑TXN ferroptotic diagnostic model with experimental validation.Molecular medicine reports · 2025Article
- Identification of sepsis biomarkers through glutamine metabolism-mediated immune regulation: a comprehensive analysis employing mendelian randomization, multi-omics integration, and machine learning.Frontiers in immunology · 2025Article
- Elucidation of neutrophils-mediated effect of MMP-2 on lung epithelial cells; implications for acute respiratory distress syndrome and severe dengue pathogenesis.Frontiers in cellular and infection microbiology · 2025Article
- Identification of CD19Journal of inflammation research · 2025Article
- Heterogeneity of Neutrophils and Immunological Function in Neonatal Sepsis: Analysis of Molecular Subtypes Based on Hypoxia-Glycolysis-Lactylation.Mediators of inflammation · 2025Article
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2 authors.
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Abstract
Introduction: Sepsis is the leading cause of death in critically ill patients; it results in multiorgan dysfunction, including acute respiratory distress syndrome (ARDS). Our study was conducted to determine the role of cellular senescence genes and immune infiltration in sepsis and sepsis-induced ARDS via bioinformatic analyses. Experimental Procedures: Datasets GSE66890 and GSE145227 were obtained from the Gene Expression Omnibus (GEO) database and utilized for bioinformatics analyses. Gene Ontology (GO) terms and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses of the differentially expressed genes (DEGs) were performed to identify the key functional modules. Two machine learning algorithms, least absolute shrinkage and selection operator (LASSO) and support vector machine recursive feature elimination (SVM-RFE), were used to screen for characteristic genes in sepsis and sepsis-induced ARDS. ROC curves were generated to evaluate the predictive ability of gene hubs. Differences in immune infiltration levels between the disease and control groups were compared via ssGSEA. The diagnostic value of the hub genes was verified via quantitative PCR (qPCR) in hospitalized patients. Results: Four characteristic genes (ATM, CCNB1, CCNA1, and E2F2) were identified as biomarkers for the progression of sepsis-induced ARDS. E2F2 showed the highest predictive ability for the occurrence of ARDS in patients with sepsis. CD56bright and plasmacytoid dendritic cells exhibited high infiltration in the sepsis-induced ARDS group, whereas eosinophils, MDSCs, macrophages, and neutrophils exhibited low infiltration. In addition, ATM expression was lower in patients with sepsis than in those without sepsis (n = 6). Conclusion: Sepsis-induced ARDS is correlated with circulating immune responses, and the expression of ATM, CCNB1, CCNA1, and E2F2 may serve as potential diagnostic biomarkers and therapeutic targets in sepsis-induced ARDS.
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