Evidence map›Paper›PMID 23388501›Full record

ArticleMultidisciplinary respiratory medicine2013

Inflammation signals airway smooth muscle cell proliferation in asthma pathogenesis.

Mohammad Afzal Khan

Open access · goldAbstract read
In one paragraph

Article in Multidisciplinary respiratory medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

33 citing papers in PubMed, 61 citations in OpenAlex.

  1. Tumor necrosis factor α-induced endoplasmic reticulum stress promotes airway smooth muscle cell proliferation.American journal of physiology. Lung cellular and molecular physiology · 2026
    Article
  2. Article
  3. Article
  4. Muscular hyperplasia in Crohn's disease strictures: through thick and thin.American journal of physiology. Cell physiology · 2024
    Review
  5. Pulmonary surfactant and prostaglandin EPhysiological reports · 2024
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Pericytes: The lung-forgotten cell type.Frontiers in physiology · 2023
    Review
  11. Article
  12. Article
  13. αJournal of personalized medicine · 2021
    Article
  14. TNFα induces mitochondrial fragmentation and biogenesis in human airway smooth muscle.American journal of physiology. Lung cellular and molecular physiology · 2021
    Article
  15. Article
  16. Review
  17. Review
  18. Regulation of IL-17A and implications for TGF-β1 comodulation of airway smooth muscle remodeling in severe asthma.American journal of physiology. Lung cellular and molecular physiology · 2019
    Article
  19. Review
  20. [Effect of acupuncture on TGF-β1/Smads pathway in mice with airway remodeling mic].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2018
    Article
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.

Mohammad Afzal KhanDepartment of Medicine, Stanford University, VAPAHCS, 3801 Miranda Avenue, Building 101, Room B4-105, Palo Alto, California, 94304, USA. afzal@stanford.edu.
Stanford University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

unlabelled

backgroundAirway inflammation stimulates proliferation of airway smooth muscle cell, which contributes to the development of hyperplasia and hypertrophy of smooth muscle cell. The increase in airway smooth muscle cell mass is believed to be due to an up-regulation of inflammatory mediators in the airway. It is now well recognized that chronic inflammation as well as airway hyper-responsiveness and remodeling of airway during inflammation, are crucial to asthma. Airway hyper-responsiveness is caused by increased cell proliferation or by hypertrophy of airway smooth muscle cell depending on the nature of the inflammatory stimulation. Airway smooth muscle cell proliferation in asthma is regulated by the proinflammatory cytokines including IL-1β and TNF-α. These proinflammatory cytokines have been shown to influence human airway smooth muscle cell proliferation in vitro, which is due to cyclooxygenase-2 expression, production of prostaglandin E2, and increased cAMP levels.

conclusionsThis review highlights the role of different proinflammatory cytokines in regulating airway smooth muscle cell growth and also focuses on regulation of differential gene expression in airway smooth muscle cell by growth factors and cytokines, also to bestow unique insight into the effects of conventional asthma therapies on airway smooth muscle cell proliferation and development of new therapeutic strategies to control asthma.

Identifiers

PMID23388501
PMCPMC3568740
OpenAlexW2138856536

What OpenQuestion holds

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LicenceCC BY
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.