ArticleBioMed research international2019
Identification of Key Pathways and Genes of Acute Respiratory Distress Syndrome Specific Neutrophil Phenotype.
Article in BioMed research international, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- The Transcription Factor DDIT3 Regulates Macrophage Function by Inhibiting KLF10 to Attenuate ALI/ARDS Inflammation.Inflammation · 2026Article
- Network analysis identifies a gene biomarker panel for sepsis-induced acute respiratory distress syndrome.BMC medical genomics · 2023Article
- Mechanistic Understanding of Lung Inflammation: Recent Advances and Emerging Techniques.Journal of inflammation research · 2022Review
- Effect and mechanism of phospholipid scramblase 4 (PLSCR4) on lipopolysaccharide (LPS)-induced injury to human pulmonary microvascular endothelial cells.Annals of translational medicine · 2021Article
- From sepsis to acute respiratory distress syndrome (ARDS): emerging preventive strategies based on molecular and genetic researches.Bioscience reports · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Despite over 50 years of clinical and basic studies, acute respiratory distress syndrome (ARDS) is still a critical challenge with high mortality worldwide. The severity of neutrophil activation was associated with disease severity. However, the detailed pathophysiology of the circulating polymorphonuclear neutrophil activation in ARDS remains unclear. To identify key pathways and genes in the ARDS-specific neutrophil phenotype distinct from sepsis, the datasets of blood polymorphonuclear neutrophils (PMNs) from patients with ARDS (GSE76293) and from sepsis patients (GSE49757) were chosen from the Gene Expression Omnibus (GEO) and analyzed using bioinformatics methods. A total of 220 differential expressed genes (DEGs) were overlapped between GSE49757 and GSE76293 in a Venn diagram. Pathway enrichment analysis results showed that DEGs in GSE76293 were mainly enriched in the MAPK signaling pathway, FoxO signaling pathway, and AMPK signaling pathway relative to GSE49757. We identified 30 hub genes in the protein-protein interaction network. By comparing with GSE49757, we speculated that GAPDH, MAPK8, PIK3CB, and MMP9 may play important roles in the progression of ARDS-specific circulating neutrophil activation. The findings may provide novel insights into the development of promising targets for the diagnosis and treatment of ARDS in the future.
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Registered trials
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