ReviewAnnals of the American Thoracic Society2014
Early events in the pathogenesis of chronic obstructive pulmonary disease. Smoking-induced reprogramming of airway epithelial basal progenitor cells.
Review in Annals of the American Thoracic Society, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.
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.
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
77 citing papers in PubMed, 114 citations in OpenAlex.
- Distinct central and peripheral airway features in bronchiolitis obliterans and COPD: an observational study.BMC pulmonary medicine · 2026Observational
- TRPC6 mediates goblet cell differentiation in COPD.Respiratory research · 2026Article
- Whole genome sequence analysis of pulmonary function and COPD in 44,287 multi-ancestry participants.Genome biology · 2026Article
- Airway basal stem cell therapy for lung diseases: an emerging regenerative medicine strategy.Stem cell research & therapy · 2025Review
- METTL3/IGF2BP2-Mediated m6A RNA Methylation Drives Alveolar Macrophage-Dependent Neutrophil Recruitment in Cigarette Smoke-Induced COPD.Journal of inflammation research · 2025Article
- Pathogenic Cell in COPD: Mechanisms of Airway Remodeling, Immune Dysregulation, and Therapeutic Implications.International journal of chronic obstructive pulmonary disease · 2025Review
- High BMP7 Expression May Worsen Airway Disease in COPD by Altering Epithelial Cell Behavior.International journal of chronic obstructive pulmonary disease · 2025Article
- Defining VOC signatures of airway epithelial cells with PM2.5 exposure.Toxicological sciences : an official journal of the Society of Toxicology · 2025Article
- Quantitative adverse outcome pathway modeling for cigarette-smoke-induced airway mucus hypersecretion. Part 1: adverse-outcome-pathway-basedFrontiers in toxicology · 2025Article
- Lung stem cells and respiratory epithelial chimerism in transplantation.European respiratory review : an official journal of the European Respiratory Society · 2025Review
- Context-dependent roles of mitochondrial LONP1 in orchestrating the balance between airway progenitor versus progeny cells.Cell stem cell · 2024Article
- Extensive airway remodelling in severe COPD imparts resiliency to environmental stressors.Thorax · 2024Article
- Roles of glutamic pyruvate transaminase 2 in reprogramming of airway epithelial lipidomic and metabolomic profiles after smoking.Clinical and translational medicine · 2024Article
- Bronchial Progenitor Cells in Obstructive and Neoplastic Lung Disease: A Pilot Study.Journal of clinical medicine · 2024Article
- Protective Effect of the Total Alkaloid Extract from BulbusInternational journal of chronic obstructive pulmonary disease · 2024Article
- Influence of cell type specific infectivity and tissue composition on SARS-CoV-2 infection dynamics within human airway epithelium.PLoS computational biology · 2023Article
- Understanding COPD Etiology, Pathophysiology, and Definition.Respiratory care · 2023Article
- Down-expression of Foxj1 on airway epithelium with impaired cilia architecture in non-cystic fibrosis bronchiectasis implies disease severity.The clinical respiratory journal · 2023Article
- The effects of epithelial-mesenchymal transitions in COPD induced by cigarette smoke: an update.Respiratory research · 2022Review
- Whole-Exome Sequencing of Bronchial Epithelial Cells Reveals a Genetic Print of Airway Remodelling in COPD.Biomedicines · 2022Article
17 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The airway epithelium is the primary site of the earliest pathologic changes induced by smoking, contributing to the development of chronic obstructive pulmonary disease (COPD). The normal human airway epithelium is composed of several major cell types, including differentiated ciliated and secretory cells, intermediate undifferentiated cells, and basal cells (BC). BC contain the stem/progenitor cell population responsible for maintenance of the normally differentiated airway epithelium. Although inflammatory and immune processes play a significant role in the pathogenesis of COPD, the earliest lesions include hyperplasia of the BC population, suggesting that the disease may start with this cell type. Apart from BC hyperplasia, smoking induces a number of COPD-relevant airway epithelial remodeling phenotypes that are likely initiated in the BC population, including mucous cell hyperplasia, squamous cell metaplasia, epithelial-mesenchymal transition, altered ciliated and nonmucous secretory cell differentiation, and suppression of junctional barrier integrity. Significant progress has been recently made in understanding the biology of human airway BC, including gene expression features, stem/progenitor, and other functions, including interaction with other airway cell types. Accumulating evidence suggests that human airway BC function as both sensors and cellular sources of various cytokines and growth factors relevant to smoking-associated airway injury, as well as the origin of various molecular and histological phenotypes relevant to the pathogenesis of COPD. In the context of these considerations, we suggest that early BC-specific smoking-induced molecular changes are critical to the pathogenesis of COPD, and these represent a candidate target for novel therapeutic approaches to prevent COPD progression in susceptible individuals.
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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.