Evidence map›Paper›PMID 22561832›Full record

ReviewNature medicine2012

The airway epithelium in asthma.

Bart N Lambrecht, Hamida Hammad

Registry-linked trialAbstract readReview
PubMed Publisher
In one paragraph

Review in Nature medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05078021 (Phenotyping Disease Severity in Asthma), which is not on this map. Cited by 438 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
438citing papers in PubMed, 1 pooled it
43.2field-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.

NCT05078021 unknown statusnot on this mapstarted 2022, after this paper: background citation

Phenotyping Disease Severity in Asthma: Molecular Investigations of Corticosteroid

TypeobservationalSponsorUniversity of CalgaryRan2022 to 2024Enrolled60ConditionsAsthmaArmsBronchoscopy
3 · Its place in the literature

Who cites it

438 citing papers in PubMed, 1 synthesis or guideline pooled it, 905 citations in OpenAlex.

  1. Pharmacological insights intoFrontiers in pharmacology · 2025
    Pooled it
  2. Trial
  3. PP4 deficiency drives airway epithelial senescence via the PERK-eIF2α-ATF4-p21 axis in severe asthma.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Vascular remodeling in asthma: from mechanisms to precision medicine.Current opinion in allergy and clinical immunology · 2026
    Review
  9. Review
  10. Review
  11. Review
  12. Asthma endotypes and theratypes.Chinese medical journal pulmonary and critical care medicine · 2026
    Review
  13. Review
  14. Repurposing approved drugs as Pendrin (Frontiers in pharmacology · 2026
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article

378 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

2 authors at 1 institution in 1 country.

Bart N LambrechtLaboratory of Immunoregulation and Mucosal Immunology, Department of Molecular Biomedical Research, VIB, Ghent, Belgium. bart.lambrecht@ugent.be
Hamida Hammad
VIB-UGent Center for Medical Biotechnology · BE

Funding

Role of Interleukin-1 in mediating epithelial-dendritic cell crosstalk in the lunR21AI083690 · NIAID · GHENT UNIVERSITY · PI HAMMAD, HAMIDA, LAMBRECHT, BART N · 2009 to 2010
$214k
NIAID NIH HHS 5R21AI083690-02
6 · The paper itself

Abstract

Asthma is a T lymphocyte-controlled disease of the airway wall caused by inflammation, overproduction of mucus and airway wall remodeling leading to bronchial hyperreactivity and airway obstruction. The airway epithelium is considered an essential controller of inflammatory, immune and regenerative responses to allergens, viruses and environmental pollutants that contribute to asthma pathogenesis. Epithelial cells express pattern recognition receptors that detect environmental stimuli and secrete endogenous danger signals, thereby activating dendritic cells and bridging innate and adaptive immunity. Improved understanding of the epithelium's function in maintaining the integrity of the airways and its dysfunction in asthma has provided important mechanistic insight into how asthma is initiated and perpetuated and could provide a framework by which to select new therapeutic strategies that prevent exacerbations and alter the natural course of the disease.

Indexed as

Airway RemodelingAllergensAnimalsAsthmaBasement MembraneCell CommunicationCytokinesDendritic CellsEpithelial CellsHumansMucusThymic Stromal LymphopoietinToll-Like Receptor 4AllergensCytokinesThymic Stromal LymphopoietinToll-Like Receptor 4

Identifiers

PMID22561832
OpenAlexW2092790181

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.