Evidence map›Paper›PMID 20008875›Full record

ReviewProceedings of the American Thoracic Society2009

The role of the epithelium in airway remodeling in asthma.

Donna E Davies

Abstract readReview
In one paragraph

Review in Proceedings of the American Thoracic Society, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers.

0numbers the graph read from it
0cells of the map it votes in
104citing papers in PubMed
10.0field-weighted citation impact, top 1% 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

104 citing papers in PubMed, 221 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. A translational view of airway epithelial dysfunction in COPD.European respiratory review : an official journal of the European Respiratory Society · 2025
    Review
  5. Review
  6. Angiogenesis Factors as Emerging Circulating Biomarkers in Asthma.Allergy, asthma & immunology research · 2025
    Review
  7. Frontiers in allergy · 2025
    Review
  8. Article
  9. The epithelial era of asthma research: knowledge gaps and future direction for patient care.European respiratory review : an official journal of the European Respiratory Society · 2024
    Review
  10. Article
  11. Article
  12. Review
  13. Review
  14. Functional role of glial-derived neurotrophic factor in a mixed allergen murine model of asthma.American journal of physiology. Lung cellular and molecular physiology · 2024
    Article
  15. Review
  16. Review
  17. Review
  18. Article
  19. DOCK2 Promotes Asthma Development by Eliciting Airway Epithelial-Mesenchymal Transition.American journal of respiratory cell and molecular biology · 2023
    Article
  20. Review

44 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.

Donna E DaviesThe Brooke Laboratories, Division of Infection, Inflammation and Immunity, University of Southampton School of Medicine, Southampton General Hospital, Southampton, United Kingdom. donnad@soton.ac.uk
Southampton General Hospital · GB

Funding

Medical Research Council G0501506Wellcome Trust
6 · The paper itself

Abstract

The bronchial epithelium is the barrier to the external environment and plays a vital role in protection of the internal milieu of the lung. It functions within the epithelial-mesenchymal trophic unit to control the local microenvironment and help maintain tissue homeostasis. However, in asthma, chronic perturbation of these homeostatic mechanisms leads to alterations in the structure of the airways, termed remodeling. Damage to the epithelium is now recognized to play a key role in driving airway remodeling. We have postulated that epithelial susceptibility to environmental stress and injury together with impaired repair responses results in generation of signals that act on the underlying mesenchyme to propagate and amplify inflammatory and remodeling responses in the submucosa. Many types of challenges to the epithelium, including pathogens, allergens, environmental pollutants, cigarette smoke, and even mechanical forces, can elicit production of mediators by the epithelium, which can be translated into remodeling responses by the mesenchyme. Several important mediators of remodeling have been identified, most notably transforming growth factor-beta, which is released from damaged/repairing epithelium or in response to inflammatory mediators, such as IL-13. The cross talk between the epithelium and the underlying mesenchyme to drive remodeling responses is considered in the context of subepithelial fibrosis and potential pathogenetic mechanisms linked to the asthma susceptibility gene, a disintegrin and metalloprotease (ADAM)33.

Indexed as

Airway RemodelingAsthmaBronchiHumansMesodermRespiratory MucosaTransforming Growth FactorsTransforming Growth Factors

Identifiers

PMID20008875
PMCPMC2797070
OpenAlexW2117559606

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.