ArticleJournal, genetic engineering & biotechnology2026
Transcriptomic landscape of airway epithelial repair: Contrasting acute and chronic injury in mustard lung and COPD.
Article in Journal, genetic engineering & biotechnology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundAirway epithelial cells play a central role in response to environmental injury and may contribute to progression from acute to chronic respiratory disease. This study investigates transcriptomic changes in airway epithelial cells following exposure to cigarette smoke and mustard gas, and compares acute injury models with chronic disease states, including COPD and mustard lung.
methodsFive airway epithelial microarray datasets were analyzed, including GSE5372 (mechanical injury; 22 samples, days 0, 7, 14), GSE20257 (COPD; 135 samples: COPD-smokers n = 23, healthy-smokers n = 53, healthy non-smokers n = 59), GSE77942 (smoke exposure; 36 samples), and two mustard-related datasets obtained from the original authors. Differential expression analysis was performed in R (limma) after normalization and filtering, using |FC| ≥ 2 and raw p ≤ 0.05. Dataset similarity was assessed by binary scoring and Pearson clustering with pvclust (100 bootstraps, AU ≥ 0.95). Functional enrichment (GO/KEGG) was performed in FunRich with Bonferroni correction, and interaction networks were analyzed using STRING (score ≥ 0.4) and visualized in Gephi.
resultsComparative transcriptomic analysis of five airway epithelial datasets revealed no differentially expressed genes shared across all conditions (|FC| ≥ 2, raw p ≤ 0.05), indicating substantial molecular divergence between acute injury models, epithelial repair processes, and chronic lung disease states. Representative examples included strong upregulation of CYP1B1 in COPD (logFC = 6.10, p = 1.31 × 10
conclusionAirway epithelial injury does not converge on a single transcriptomic signature but instead follows distinct condition-specific programs. Across datasets, EMT/MET-associated gene expression and extracellular matrix remodeling emerged as central processes linking acute injury, epithelial repair, and chronic airway disease. These findings suggest that dysregulated epithelial repair mechanisms may drive persistent airway remodeling in COPD and mustard lung, highlighting EMT-associated pathways as potential targets for future investigation.
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