Evidence map›Paper›PMID 23577039›Full record

ArticleJournal of allergy2013

Airway smooth muscle hypercontractility in asthma.

Rachid Berair, Fay Hollins, Christopher Brightling

Open access · hybridAbstract read
In one paragraph

Article in Journal of allergy, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

22 citing papers in PubMed, 41 citations in OpenAlex.

  1. Review
  2. Article
  3. Downregulation of protein phosphatase 2Aα in asthmatic airway smooth muscle.American journal of physiology. Lung cellular and molecular physiology · 2024
    Article
  4. Article
  5. Article
  6. Airway smooth muscle function in asthma.Frontiers in physiology · 2022
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. TGF-β1 Evokes Human Airway Smooth Muscle Cell Shortening and Hyperresponsiveness via Smad3.American journal of respiratory cell and molecular biology · 2018
    Article
  12. Article
  13. A novel role for primary cilia in airway remodeling.American journal of physiology. Lung cellular and molecular physiology · 2017
    Article
  14. Review
  15. Highly selective inhibition of myosin motors provides the basis of potential therapeutic application.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  16. Giant Cell Arteritis: From Pathogenesis to Therapeutic Management.Current treatment options in rheumatology · 2016
    Article
  17. The impact of vitamin D on asthmatic human airway smooth muscle.Expert review of respiratory medicine · 2016
    Article
  18. Article
  19. Article
  20. Review
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 at 1 institution in 1 country.

Rachid BerairDepartment of Infection, Inflammation and Immunity, Institute for Lung Health, University of Leicester, Leicester LE3 9QP, UK.
Fay Hollins
Christopher Brightling
University of Leicester · GB

Funding

Wellcome Trust 082265
6 · The paper itself

Abstract

In recent years, asthma has been defined primarily as an inflammatory disorder with emphasis on inflammation being the principle underlying pathophysiological characteristic driving airway obstruction and remodelling. Morphological abnormalities of asthmatic airway smooth muscle (ASM), the primary structure responsible for airway obstruction seen in asthma, have long been described, but surprisingly, until recently, relatively small number of studies investigated whether asthmatic ASM was also fundamentally different in its functional properties. Evidence from recent studies done on single ASM cells and on ASM-impregnated gel cultures have shown that asthmatic ASM is intrinsically hypercontractile. Several elements of the ASM contraction apparatus in asthmatics and in animal models of asthma have been found to be different from nonasthmatics. These differences include some regulatory contractile proteins and also some components of both the calcium-dependent and calcium-independent contraction signalling pathways. Furthermore, oxidative stress was also found to be heightened in asthmatic ASM and contributes to hypercontractility. Understanding the abnormalities and mechanisms driving asthmatic ASM hypercontractility provides a great potential for the development of new targeted drugs, other than the conventional current anti-inflammatory and bronchodilator therapies, to address the desperate unmet need especially in patients with severe and persistent asthma.

Identifiers

PMID23577039
PMCPMC3613096
OpenAlexW2048654643

What OpenQuestion holds

Textmetadata
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.