Evidence map›Paper›PMID 25354273›Full record

ArticleAmerican journal of respiratory and critical care medicine2014

Airway basal cells. The "smoking gun" of chronic obstructive pulmonary disease.

Ronald G Crystal

Open access · greenAbstract read
In one paragraph

Article in American journal of respiratory and critical care medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers.

0numbers the graph read from it
0cells of the map it votes in
87citing papers in PubMed
4.6field-weighted citation impact, top 5% 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

87 citing papers in PubMed, 132 citations in OpenAlex.

  1. Autologous transplantation of P63Cell reports. Medicine · 2024
    Trial
  2. Review
  3. Air pollution-induced airway epithelial barrier dysfunction in COPD: a narrative review of mechanisms and therapeutic implications.European respiratory review : an official journal of the European Respiratory Society · 2026
    Review
  4. Article
  5. Article
  6. Article
  7. A translational view of airway epithelial dysfunction in COPD.European respiratory review : an official journal of the European Respiratory Society · 2025
    Review
  8. Article
  9. Review
  10. Review
  11. Engineered hydrogel biomaterials facilitate lung progenitor cell differentiation from induced pluripotent stem cells.American journal of physiology. Lung cellular and molecular physiology · 2025
    Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
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  20. Review

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

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

Ronald G CrystalDepartment of Genetic Medicine, Weill Cornell Medical College, New York, New York.
Cornell University · US

Funding

Overlapping Airway Basal Cell Transcriptome Reprogramming in COPD and Lung CancerR01HL107882 · NHLBI · WEILL MEDICAL COLL OF CORNELL UNIV · PI CRYSTAL, RONALD G · 2011 to 2014
$5.8M
COPD Metabolome, Smoking Oxidants and Aberrant Ciliated Cell FunctionP20HL113443 · NHLBI · WEILL MEDICAL COLL OF CORNELL UNIV · PI CRYSTAL, RONALD G · 2012 to 2016
$5.3M
Integrative-omics Network Model of the Disordered COPD Small Airway EpitheliumR01HL118541 · NHLBI · WEILL MEDICAL COLL OF CORNELL UNIV · PI CRYSTAL, RONALD G, MEZEY, JASON G · 2014 to 2017
$3.9M
NHLBI NIH HHS HL118541NHLBI NIH HHS P20 HL113443NHLBI NIH HHS R01 HL107882NHLBI NIH HHS R01HL107882NHLBI NIH HHS R01 HL118541
6 · The paper itself

Abstract

The earliest abnormality in the lung associated with smoking is hyperplasia of airway basal cells, the stem/progenitor cells of the ciliated and secretory cells that are central to pulmonary host defense. Using cell biology and 'omics technologies to assess basal cells isolated from bronchoscopic brushings of nonsmokers, smokers, and smokers with chronic obstructive pulmonary disease (COPD), compelling evidence has been provided in support of the concept that airway basal cells are central to the pathogenesis of smoking-associated lung diseases. When confronted by the chronic stress of smoking, airway basal cells become disorderly, regress to a more primitive state, behave as dictated by their inheritance, are susceptible to acquired changes in their genome, lose the capacity to regenerate the epithelium, are responsible for the major changes in the airway that characterize COPD, and, with persistent stress, can undergo malignant transformation. Together, these observations led to the conclusion that accelerated loss of lung function in susceptible individuals begins with disordered airway basal cell biology (i.e., that airway basal cells are the "smoking gun" of COPD, a potential target for the development of therapies to prevent smoking-related lung disorders).

Indexed as

HumansLungLung NeoplasmsPulmonary Disease, Chronic ObstructiveRespiratory MucosaSmokingStem Cellsairway epitheliumbasal cellsCOPDlung cancersmoking

Identifiers

PMID25354273
PMCPMC4299651
OpenAlexW2162828739

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.