ArticleBMC infectious diseases2021
Identification of significant alteration genes, pathways and TFs induced by LPS in ARDS via bioinformatical analysis.
Article in BMC infectious diseases, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 9 citations in OpenAlex.
- Epithelial plasticity shapes intratumoral heterogeneity and cell lineages in early-stage lung cancer.Science advances · 2026Article
- Leptin, vitamin D, and APRI values during the six months post-liver transplantation.BMC gastroenterology · 2026Article
- IFIT3 stabilizes STING via USP18 to drive M1 macrophage polarization and early inflammation in acute lung injury.Cellular and molecular life sciences : CMLS · 2026Article
- Pathophysiological mechanisms of ARDS: a narrative review from molecular to organ-level perspectives.Respiratory research · 2025Review
- From mechanisms to therapies: the multifaceted roles of guanylate-binding protein 2 in immunity, cancer, and beyond.Frontiers in immunology · 2025Review
- Type I IFN receptor blockade alleviates liver fibrosis through macrophage-derived STAT3 signaling.Frontiers in immunology · 2025Article
- Trimethoprim-sulfamethoxazole acute respiratory distress syndrome requiring lung transplantation.Respirology case reports · 2024Article
- Genetic Determinants of the Acute Respiratory Distress Syndrome.Journal of clinical medicine · 2023Review
- Upregulation ofAnnals of translational medicine · 2022Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND AND
aimsAcute respiratory distress syndrome (ARDS) or acute lung injury (ALI) is one of the most common acute thoracopathy with complicated pathogenesis in ICU. The study is to explore the differentially expressed genes (DEGs) in the lung tissue and underlying altering mechanisms in ARDS.
methodsGene expression profiles of GSE2411 and GSE130936 were available from GEO database, both of them included in GPL339. Then, an integrated analysis of these genes was performed, including gene ontology (GO) and KEGG pathway enrichment analysis in DAVID database, protein-protein interaction (PPI) network construction evaluated by the online database STRING, Transcription Factors (TFs) forecasting based on the Cytoscape plugin iRegulon, and their expression in varied organs in The Human Protein Atlas.
resultsA total of 39 differential expressed genes were screened from the two datasets, including 39 up-regulated genes and 0 down-regulated genes. The up-regulated genes were mainly enriched in the biological process, such as immune system process, innate immune response, inflammatory response, and also involved in some signal pathways, including cytokine-cytokine receptor interaction, Salmonella infection, Legionellosis, Chemokine, and Toll-like receptor signal pathway with an integrated analysis. GBP2, IFIT2 and IFIT3 were identified as hub genes in the lung by PPI network analysis with MCODE plug-in, as well as GO and KEGG re-enrichment. All of the three hub genes were regulated by the predictive common TFs, including STAT1, E2F1, IRF1, IRF2, and IRF9.
conclusionsThis study implied that hub gene GBP2, IFIT2 and IFIT3, which might be regulated by STAT1, E2F1, IRF1, IRF2, or IRF9, played significant roles in ARDS. They could be potential diagnostic or therapeutic targets for ARDS patients.
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