ArticlePloS one2016
Cigarette Smoke Enhances the Expression of Profibrotic Molecules in Alveolar Epithelial Cells.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 3 of them syntheses that pooled it.
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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.
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Who cites it
35 citing papers in PubMed, 3 syntheses or guidelines pooled it, 67 citations in OpenAlex.
- Incidence and predictors of acute respiratory distress syndrome in sepsis: a systematic review and meta-analysis.Frontiers in medicine · 2026Pooled it
- Organizing mechanism-related information on chemical interactions using a framework based on the aggregate exposure and adverse outcome pathways.Environment international · 2020Pooled it
- The Association between Smoking and Epiretinal Membrane.Scientific reports · 2016Pooled it
- Transcriptomic landscape of airway epithelial repair: Contrasting acute and chronic injury in mustard lung and COPD.Journal, genetic engineering & biotechnology · 2026Article
- Smoker's Lungs: Quo Vadis? Exploring the Shared and Individual Smoking-Related Molecular Pathways of Emphysema, Carcinoma, and Fibrosis - An Illustrative Review.Thoracic cancer · 2026Review
- Irisin maintains ER homeostasis and activates AMPK via integrin αVβ5 to attenuate CSE + LPS-induced emphysema and inflammation.Respiratory research · 2026Article
- Antifibrotic Effects ofInternational journal of molecular sciences · 2026Article
- Integrins and pulmonary fibrosis: Pathogenic roles and therapeutic opportunities.Biomolecules & biomedicine · 2025Review
- A next-generation system for smoke inhalation integrated with a breathing lung-on-chip to model human lung responses to cigarette exposure.Scientific reports · 2025Article
- ITGAV, a specific biomarker associated with the pathogenesis of idiopathic pulmonary fibrosis.Scientific reports · 2025Article
- Adoptive Transfer of T Cells as a Potential Therapeutic Approach in the Bleomycin-Injured Mouse Lung.The journal of gene medicine · 2025Article
- Deciphering the interplay: circulating cell-free DNA, signaling pathways, and disease progression in idiopathic pulmonary fibrosis.3 Biotech · 2025Review
- Comparative Evaluation of Cigarette Smoke and a Heated Tobacco Product on Corneal Oxidative Stress in an Air/Liquid Interface Model.Investigative ophthalmology & visual science · 2025Article
- Oxidative Stress and Lung Fibrosis: Towards an Adverse Outcome Pathway.International journal of molecular sciences · 2023Review
- mRNA Levels of Epithelial and Mesenchymal Markers in Lung Epithelial Cell Lines.Reports of biochemistry & molecular biology · 2023Article
- Genomic Fingerprint Associated with Familial Idiopathic Pulmonary Fibrosis: A Review.International journal of medical sciences · 2023Review
- Bacterial biomarkers capable of identifying recurrence or metastasis carry disease severity information for lung cancer.Frontiers in microbiology · 2022Article
- The role of cancer stromal fibroblasts in mediating the effects of tobacco-induced cancer cell growth.Cancer cell international · 2021Review
- Involvement of the ACE2/Ang-(1-7)/MasR Axis in Pulmonary Fibrosis: Implications for COVID-19.International journal of molecular sciences · 2021Review
- Targeting the AXL Receptor in Combating Smoking-related Pulmonary Fibrosis.American journal of respiratory cell and molecular biology · 2021Article
Corrections and comments
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Authors and funding
14 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Idiopathic pulmonary fibrosis (IPF) is a progressive and lethal disease of unknown etiology. A growing body of evidence indicates that it may result from an aberrant activation of alveolar epithelium, which induces the expansion of the fibroblast population, their differentiation to myofibroblasts and the excessive accumulation of extracellular matrix. The mechanisms that activate the alveolar epithelium are unknown, but several studies indicate that smoking is the main environmental risk factor for the development of IPF. In this study we explored the effect of cigarette smoke on the gene expression profile and signaling pathways in alveolar epithelial cells. Lung epithelial cell line from human (A549), was exposed to cigarette smoke extract (CSE) for 1, 3, and 5 weeks at 1, 5 and 10% and gene expression was evaluated by complete transcriptome microarrays. Signaling networks were analyzed with the Ingenuity Pathway Analysis software. At 5 weeks of exposure, alveolar epithelial cells acquired a fibroblast-like phenotype. At this time, gene expression profile revealed a significant increase of more than 1000 genes and deregulation of canonical signaling pathways such as TGF-β and Wnt. Several profibrotic genes involved in EMT were over-expressed, and incomplete EMT was observed in these cells, and corroborated in mouse (MLE-12) and rat (RLE-6TN) epithelial cells. The secretion of activated TGF-β1 increased in cells exposed to cigarette smoke, which decreased when the integrin alpha v gene was silenced. These findings suggest that the exposure of alveolar epithelial cells to CSE induces the expression and release of a variety of profibrotic genes, and the activation of TGF-β1, which may explain at least partially, the increased risk of developing IPF in smokers.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.