ArticleEuropean journal of medical research2024
Gene expression profile analysis of severe influenza-based modulation of idiopathic pulmonary fibrosis.
Article in European journal of medical research, 2024. 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.
- The cell with many faces: lung macrophage plasticity and function in response to environmental and pathogenic insults.Physiological reviews · 2026Review
- Article
- Low-level red light inhibits human retinal pigment epithelial cell fibrosis via UBE2C in a myopia-simulating hypoxic microenvironment.European journal of medical research · 2025Article
- Integrating machine learning with bioinformatics for predicting idiopathic pulmonary fibrosis prognosis: developing an individualized clinical prediction tool.Experimental biology and medicine (Maywood, N.J.) · 2024Article
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2 authors.
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Abstract
backgroundIt is known severe influenza infections and idiopathic pulmonary fibrosis (IPF) disease might stimulate each other. Till now, no associated mechanism has been reported.
methodWe collected the genetic pattern of expression of severe influenza (GSE111368) and IPF (GSE70866) from the Gene Expression Omnibus (GEO) database. Common differentially expressed genes (C-DEGs) were identified from the two datasets, and using this data, we conducted three forms of analyses, functional annotation, protein-protein interaction (PPI) network and module construction, and hub gene identification and co-expression analysis.
resultsIn all, 174 C-DEGs were selected for additional analyses. Based on our functional analysis, these C-DEGs mediated inflammatory response and cell differentiation. Furthermore, using cytoHubba, we identified 15 genes, namely, MELK, HJURP, BIRC5, TPX2, TK1, CDT1, UBE2C, UHRF1, CCNA2, TYMS, CDCA5, CDCA8, RAD54L, CCNB2, and ITGAM, which served as hub genes to possibly contribute to severe influenza patients with IPF disease as comorbidity. The hub gene expressions were further confirmed using two stand-alone datasets (GSE101702 for severe influenza and GSE10667 for IPF).
conclusionHerein, we demonstrated the significance of common pathways and critical genes in severe influenza and IPF etiologies. The identified pathways and genes may be employed as possible therapeutic targets for future therapy against severe influenza patients with IPF.
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