ArticleScientific reports2025
Autophagy-related biomarkers identified in sepsis-induced ARDS through bioinformatics analysis.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- ADAMTS2 Modulates Inflammation, Autophagy, and Barrier Integrity Through PI3K/AKT/mTOR Signaling in LPS-Induced Acute Respiratory Distress Syndrome.Immunity, inflammation and disease · 2026Article
- Mechanisms and therapeutics of immunometabolic reprogramming driving macrophage-ECs interactions in sepsis-associated ARDS from the gut-lung axis perspective.Frontiers in immunology · 2026Review
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
While dysregulated autophagy has been linked to acute respiratory distress syndrome (ARDS) development in sepsis, the exact regulatory mechanisms driving this process remain unclear. This study systematically investigated autophagy-related genes in sepsis-induced ARDS using integrative bioinformatics, including weighted gene coexpression network analysis (WGCNA), differential gene expression analysis (DEGs), receiver operating characteristic (ROC) curve analysis, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis, protein‒protein interaction (PPI) network analysis, and immune infiltration analysis. Hub genes were further validated by qPCR in Beas-2B cells receiving lipopolysaccharide (LPS) stimulation. We identified 18 autophagy-related DEGs with diagnostic potential for sepsis-induced ARDS. These DEGs were linked to endocytosis, protein kinase inhibition, and enigmatic Ficolin-1-rich granules. The downregulated hallmark signaling pathways involved apoptosis, complement, IL-2/STAT5, and KRAS signaling. Immune infiltration analysis revealed alterations in 7 immune cell subsets, including CD8 + T-cell exhaustion, natural killer cell reduction, and the type 1 helper T-cell response. When Beas-2B cells were treated with LPS, we discovered that 6 out of the 18 hub genes were significantly downregulated. Our findings provide novel insights into autophagy-mediated ARDS pathogenesis in sepsis. The hub genes represent promising candidates for clinical biomarker development and therapeutic targeting, which necessitates further validation.
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Registered trials
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