Evidence map›Paper›PMID 26998246›Full record

ReviewF1000Research2016

Airway hyperresponsiveness; smooth muscle as the principal actor.

Anne-Marie Lauzon, James G Martin

Open access · goldAbstract readReview
In one paragraph

Review in F1000Research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
5.5field-weighted citation impact, top 4% 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

31 citing papers in PubMed, 61 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Photobiomodulation Mitigates PMAntioxidants (Basel, Switzerland) · 2024
    Article
  6. Review
  7. Article
  8. Review
  9. OGR1-dependent regulation of the allergen-induced asthma phenotype.American journal of physiology. Lung cellular and molecular physiology · 2021
    Article
  10. Review
  11. Article
  12. Airway mechanical compression: its role in asthma pathogenesis and progression.European respiratory review : an official journal of the European Respiratory Society · 2020
    Review
  13. Airway smooth muscle tone increases actin filamentogenesis and contractile capacity.American journal of physiology. Lung cellular and molecular physiology · 2020
    Article
  14. Review
  15. Metabolic Adaptation of Airway Smooth Muscle Cells to an SPHK2 Substrate Precedes Cytostasis.American journal of respiratory cell and molecular biology · 2020
    Article
  16. Review
  17. Article
  18. Review
  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

2 authors at 1 institution in 1 country.

Anne-Marie LauzonMeakins-Christie Laboratories, McGill University Health Center Research Institute, Montreal, QC, Canada; Department of Medicine, McGill University, Montreal, QC, Canada.
James G MartinMeakins-Christie Laboratories, McGill University Health Center Research Institute, Montreal, QC, Canada; Department of Medicine, McGill University, Montreal, QC, Canada.
McGill University · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Airway hyperresponsiveness (AHR) is a defining characteristic of asthma that refers to the capacity of the airways to undergo exaggerated narrowing in response to stimuli that do not result in comparable degrees of airway narrowing in healthy subjects. Airway smooth muscle (ASM) contraction mediates airway narrowing, but it remains uncertain as to whether the smooth muscle is intrinsically altered in asthmatic subjects or is responding abnormally as a result of the milieu in which it sits. ASM in the trachea or major bronchi does not differ in its contractile characteristics in asthmatics, but the more pertinent peripheral airways await complete exploration. The mass of ASM is increased in many but not all asthmatics and therefore cannot be a unifying hypothesis for AHR, although when increased in mass it may contribute to AHR. The inability of a deep breath to reverse or prevent bronchial narrowing in asthma may reflect an intrinsic difference in the mechanisms that lead to softening of contracted ASM when subjected to stretch. Cytokines such as interleukin-13 and tumor necrosis factor-α promote a more contractile ASM phenotype. The composition and increased stiffness of the matrix in which ASM is embedded promotes a more proliferative and pro-inflammatory ASM phenotype, but the expected dedifferentiation and loss of contractility have not been shown. Airway epithelium may drive ASM proliferation and/or molecular remodeling in ways that may lead to AHR. In conclusion, AHR is likely multifactorial in origin, reflecting the plasticity of ASM properties in the inflammatory environment of the asthmatic airway.

Indexed as

Airway epitheliumAirway hyperresponsivenessasthmasmooth muscle

Identifiers

PMID26998246
PMCPMC4786946
OpenAlexW2341117108

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.