ArticlePloS one2014
Smoking dysregulates the human airway basal cell transcriptome at COPD risk locus 19q13.2.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.
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.
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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
47 citing papers in PubMed, 1 synthesis or guideline pooled it, 73 citations in OpenAlex.
- Pooled it
- Nasal epithelium and blood transcriptomic signatures associations with smoking and exacerbations.The European respiratory journal · 2026Article
- Identification of Biomarkers and Molecular Pathways Implicated in Smoking and COVID-19 Associated Lung Cancer Using Bioinformatics and Machine Learning Approaches.International journal of environmental research and public health · 2024Article
- Physiological and immunological barriers in the lung.Seminars in immunopathology · 2024Review
- Serial Sampling of the Small Airway Epithelium to Identify Persistent Smoking-dysregulated Genes.American journal of respiratory and critical care medicine · 2023Article
- The pathogenetic influence of smoking on SARS-CoV-2 infection: Integrative transcriptome and regulomics analysis of lung epithelial cells.Computers in biology and medicine · 2023Article
- Article
- Inflammatory Alveolar Type 2 Cells in Chronic Obstructive Pulmonary Disease: Impairing or Improving Disease Outcome?American journal of respiratory cell and molecular biology · 2022Article
- Statistical Bioinformatics to Uncover the Underlying Biological Mechanisms That Linked Smoking with Type 2 Diabetes Patients Using Transcritpomic and GWAS Analysis.Molecules (Basel, Switzerland) · 2022Article
- Senescence: Pathogenic Driver in Chronic Obstructive Pulmonary Disease.Medicina (Kaunas, Lithuania) · 2022Review
- Nicotine dose-dependent epigenomic-wide DNA methylation changes in the mice with long-term electronic cigarette exposure.American journal of cancer research · 2022Article
- Fiberoptic Bronchoscopic Findings in Patients Suffering from Emerging Pulmonary Lophomoniasis: A First Registry-Based Clinical Study.Interdisciplinary perspectives on infectious diseases · 2022Article
- Mainstream Cigarette Smoke Impacts the Mouse Vocal Fold Epithelium and Mucus Barrier.The Laryngoscope · 2021Observational
- Cellular and functional heterogeneity of the airway epithelium.Mucosal immunology · 2021Review
- Impaired Differentiation of Chronic Obstructive Pulmonary Disease Bronchial Epithelial Cells Grown on Bronchial Scaffolds.American journal of respiratory cell and molecular biology · 2021Article
- Cigarette Smoke Specifically Affects Small Airway Epithelial Cell Populations and Triggers the Expansion of Inflammatory and Squamous Differentiation Associated Basal Cells.International journal of molecular sciences · 2021Article
- LTBP4 in Health and Disease.Genes · 2021Review
- The optimal discovery procedure for significance analysis of general gene expression studies.Bioinformatics (Oxford, England) · 2021Article
- Short-term whole body cigarette smoke exposure induces regional differences in cellular response in the mouse larynx.Toxicology reports · 2021Article
- Microarray analysis identifies defects in regenerative and immune response pathways in COPD airway basal cells.ERJ open research · 2020Article
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
Abstract
Genome-wide association studies (GWAS) and candidate gene studies have identified a number of risk loci associated with the smoking-related disease COPD, a disorder that originates in the airway epithelium. Since airway basal cell (BC) stem/progenitor cells exhibit the earliest abnormalities associated with smoking (hyperplasia, squamous metaplasia), we hypothesized that smoker BC have a dysregulated transcriptome, enriched, in part, at known GWAS/candidate gene loci. Massive parallel RNA sequencing was used to compare the transcriptome of BC purified from the airway epithelium of healthy nonsmokers (n = 10) and healthy smokers (n = 7). The chromosomal location of the differentially expressed genes was compared to loci identified by GWAS to confer risk for COPD. Smoker BC have 676 genes differentially expressed compared to nonsmoker BC, dominated by smoking up-regulation. Strikingly, 166 (25%) of these genes are located on chromosome 19, with 13 localized to 19q13.2 (p<10⁻⁴ compared to chance), including 4 genes (NFKBIB, LTBP4, EGLN2 and TGFB1) associated with risk for COPD. These observations provide the first direct connection between known genetic risks for smoking-related lung disease and airway BC, the population of lung cells that undergo the earliest changes associated with smoking.
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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.