Autophagy-related biomarkers identified in sepsis-induced ARDS through bioinformatics analysis.
Summary
Integrative transcriptomic analyses identified 18 autophagy-related differentially expressed genes in sepsis-induced ARDS, with pathway links to endocytosis and immune signaling. qPCR in LPS-stimulated Beas-2B cells confirmed downregulation of 6 hub genes, nominating candidates for biomarker development and therapeutic targeting.
Key Findings
- Identified 18 autophagy-related DEGs in sepsis-induced ARDS via WGCNA, DEGs, and PPI analyses with ROC-based diagnostic potential.
- Pathway analyses implicated endocytosis, apoptosis, complement, IL-2/STAT5, and KRAS signaling alterations.
- qPCR validation in LPS-stimulated Beas-2B cells confirmed significant downregulation of 6 hub genes.
Clinical Implications
If validated clinically, the identified hub genes could support early diagnosis, risk stratification, and selection of patients for autophagy-modulating therapies in sepsis-induced ARDS.
Why It Matters
Provides mechanistic leads and a prioritized gene list for sepsis-induced ARDS, advancing pathophysiology and biomarker discovery. The multi-method pipeline is broadly reusable across diseases.
Limitations
- Clinical sample size and cohorts are not detailed; lack of external patient-level validation
- Validation limited to a single bronchial epithelial cell line and acute LPS stimulation model
Future Directions
Prospective patient cohort validation with protein-level assays, tissue localization, and functional perturbation studies of candidate genes in in vivo ARDS models.
Study Information
- Study Type
- Case-control
- Research Domain
- Pathophysiology
- Evidence Level
- V - Preclinical/in silico discovery study with limited in vitro validation; no clinical intervention.
- Study Design
- OTHER