Evidence map›Paper›PMID 29211494›Full record

ArticleAmerican journal of respiratory and critical care medicine2018

Exhaustion of Airway Basal Progenitor Cells in Early and Established Chronic Obstructive Pulmonary Disease.

Moumita Ghosh, York E Miller, Ichiro Nakachi, Jennifer B Kwon, Anna E Barón, Alexandra E Brantley, Daniel T Merrick, Wilbur A Franklin, Robert L Keith, R William Vandivier

Abstract read
In one paragraph

Article in American journal of respiratory and critical care medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.

0numbers the graph read from it
0cells of the map it votes in
76citing papers in PubMed
7.8field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

76 citing papers in PubMed, 120 citations in OpenAlex.

  1. Article
  2. Article
  3. Hallmarks of the ageing lung: 10 years later.The European respiratory journal · 2026
    Review
  4. Progenitor Resilience and the Early Onset of Chronic Lung Diseases: NHLBI workshop report.American journal of respiratory cell and molecular biology · 2026
    Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
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  12. Mechanisms and markers of lung ageing in health and disease.European respiratory review : an official journal of the European Respiratory Society · 2025
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. Article

16 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 6 institutions in 2 countries.

Moumita Ghosh1 Division of Pulmonary, Critical Care and Sleep Medicine, Department of Medicine, National Jewish Health, Denver, Colorado.
York E Miller2 COPD Program, Division of Pulmonary Sciences and Critical Care Medicine, Department of Medicine, and.
Ichiro Nakachi4 Division of Pulmonary Medicine, Department of Medicine, Keio University School of Medicine, Tokyo, Japan; and.
Jennifer B Kwon1 Division of Pulmonary, Critical Care and Sleep Medicine, Department of Medicine, National Jewish Health, Denver, Colorado.
Anna E Barón5 Department of Biostatistics and Bioinformatics, University of Colorado School of Public Health, Aurora, Colorado.
Alexandra E Brantley1 Division of Pulmonary, Critical Care and Sleep Medicine, Department of Medicine, National Jewish Health, Denver, Colorado.
Daniel T Merrick6 Department of Pathology, University of Colorado Anschutz Medical Campus, Aurora, Colorado.
Wilbur A Franklin6 Department of Pathology, University of Colorado Anschutz Medical Campus, Aurora, Colorado.
Robert L Keith2 COPD Program, Division of Pulmonary Sciences and Critical Care Medicine, Department of Medicine, and.
R William Vandivier2 COPD Program, Division of Pulmonary Sciences and Critical Care Medicine, Department of Medicine, and.
National Jewish Health · USUniversity of Colorado Anschutz Medical Campus · USVA Eastern Colorado Health Care System · USColorado School of Public Health · USKeio University · JPPulmonary and Critical Care Associates · US

Funding

University of Colorado Cancer Center Support Grant - Lung Cancer Patient-Derived Xenografts with Autologous Human Immune SystemsP30CA046934 · NCI · UNIVERSITY OF COLORADO DENVER · PI James V Degregori · 1988 to 2026
$117.0M
Tissue Bank and Biomarkers CoreP50CA058187 · NCI · UNIVERSITY OF COLORADO DENVER · PI MILLER, YORK E · 1992 to 2018
$43.8M
(PQ1) Progenitor cell malfunction, mutations and changes in microenvironment: A dynamic risk spectrum for cancer evolutionR01CA219893 · NCI · UNIVERSITY OF COLORADO DENVER · PI GHOSH, MOUMITA, MILLER, YORK E · 2017 to 2022
$2.3M
Exhaustion of Airway Progenitor Cells Indicates Susceptibility to COPDR01HL129938 · NHLBI · NATIONAL JEWISH HEALTH · PI GHOSH, MOUMITA · 2015 to 2017
$1.2M
PPAR gamma Agonists for Lung Cancer ChemopreventionI01BX000382 · VA · VA EASTERN COLORADO HEALTH CARE SYSTEM · PI KEITH, ROBERT · 2011 to 2020
–
BLRD VA I01 BX000382NCI NIH HHS P30 CA046934NCI NIH HHS P50 CA058187NCI NIH HHS R01 CA219893NHLBI NIH HHS R01 HL129938
6 · The paper itself

Abstract

rationaleUp to 40% of smokers develop chronic obstructive pulmonary disease (COPD) over a period that spans decades. Despite the importance of COPD, much remains to be learned about susceptibility and pathogenesis, especially during early, prediagnostic stages of disease. Airway basal progenitor cells are crucial for lung health and resilience because of their ability to repair injured airways. In COPD, the normal airway epithelium is replaced with increased basal and secretory (mucous) cells and decreased ciliated cells, suggesting that progenitors are impaired.

objectivesTo examine airway basal progenitor cells and lung function in smokers with and without COPD.

methodsBronchial biopsies taken from smokers at risk for COPD and lung cancer were used to acquire airway basal progenitor cells. They were evaluated for count, self-renewal, and multipotentiality (ability to differentiate to basal, mucous, and ciliated cells), and progenitor count was examined for its relationship with lung function. MEASUREMENTS AND MAIN

resultsBasal progenitor count, self-renewal, and multipotentiality were all reduced in COPD versus non-COPD. COPD progenitors produced an epithelium with increased basal and mucous cells and decreased ciliated cells, replicating the COPD phenotype. Progenitor depletion correlated with lung function and identified a subset of subjects without COPD with lung function that was midway between non-COPD with high progenitor counts and those with COPD.

conclusionsBasal progenitor dysfunction relates to the histologic and physiologic manifestations of COPD and identifies a subset that may represent an early, prediagnostic stage of COPD, indicating that progenitor exhaustion is involved in COPD pathogenesis.

Indexed as

BiopsyCross-Sectional StudiesDisease ProgressionEpitheliumFemaleHumansLungMaleMiddle AgedPulmonary Disease, Chronic ObstructiveSeverity of Illness IndexSmokersSmokingStem CellsTimecell self-renewaldisease susceptibilityearly diagnosismultipotentialitystem cells

Identifiers

PMID29211494
PMCPMC6020409
OpenAlexW2773963595

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.