Evidence map›Paper›PMID 24032029›Full record

ReviewFrontiers in microbiology2013

Pathology of asthma.

Makoto Kudo, Yoshiaki Ishigatsubo, Ichiro Aoki

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Frontiers in microbiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 146 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
146citing papers in PubMed, 6 pooled it
–field-weighted citation impact
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

146 citing papers in PubMed, 6 syntheses or guidelines pooled it.

  1. A molecular systems architecture of asthma.Frontiers in immunology · 2026
    Pooled it
  2. Pooled it
  3. Pooled it
  4. Association between Val66Met polymorphisms in brain-derived neurotrophic factor gene and asthma risk: a meta-analysis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2015
    Pooled it
  5. Pooled it
  6. Pooled it
  7. Trial
  8. Trial
  9. Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. Participation of miRNA-23a-3p in Pulmonary Tuberculosis Through Macrophages via the JAK-STAT Pathway.International journal of chronic obstructive pulmonary disease · 2026
    Article
  16. Deciphering the Tenascin-C Nexus: A Comprehensive Review of Its Involvement in Chronic Respiratory Diseases.Pathophysiology : the official journal of the International Society for Pathophysiology · 2025
    Review
  17. Article
  18. Beyond classical collagen: basement membrane collagen IV in age-associated lung diseases.European respiratory review : an official journal of the European Respiratory Society · 2025
    Review
  19. Article
  20. Review

86 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

3 authors.

Makoto KudoDepartment of Clinical Immunology and Internal medicine, Graduate School of Medicine, Yokohama City University Yokohama, Japan.
Yoshiaki Ishigatsubo
Ichiro Aoki

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Asthma is a serious health and socioeconomic issue all over the world, affecting more than 300 million individuals. The disease is considered as an inflammatory disease in the airway, leading to airway hyperresponsiveness, obstruction, mucus hyper-production and airway wall remodeling. The presence of airway inflammation in asthmatic patients has been found in the nineteenth century. As the information in patients with asthma increase, paradigm change in immunology and molecular biology have resulted in an extensive evaluation of inflammatory cells and mediators involved in the pathophysiology of asthma. Moreover, it is recognized that airway remodeling into detail, characterized by thickening of the airway wall, can be profound consequences on the mechanics of airway narrowing and contribute to the chronic progression of the disease. Epithelial to mesenchymal transition plays an important role in airway remodeling. These epithelial and mesenchymal cells cause persistence of the inflammatory infiltration and induce histological changes in the airway wall, increasing thickness of the basement membrane, collagen deposition and smooth muscle hypertrophy and hyperplasia. Resulting of airway inflammation, airway remodeling leads to the airway wall thickening and induces increased airway smooth muscle mass, which generate asthmatic symptoms. Asthma is classically recognized as the typical Th2 disease, with increased IgE levels and eosinophilic inflammation in the airway. Emerging Th2 cytokines modulates the airway inflammation, which induces airway remodeling. Biological agents, which have specific molecular targets for these Th2 cytokines, are available and clinical trials for asthma are ongoing. However, the relatively simple paradigm has been doubted because of the realization that strategies designed to suppress Th2 function are not effective enough for all patients in the clinical trials. In the future, it is required to understand more details for phenotypes of asthma.

Indexed as

asthmacytokinesepithelial to mesenchymal transitionremodelingTh17 cellsTh2 cellsTh9 cell

Identifiers

PMID24032029
PMCPMC3768124

What OpenQuestion holds

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LicenceCC BY
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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.