Evidence map›Paper›PMID 17463392›Full record

ArticleAmerican journal of respiratory cell and molecular biology2007

Airway hyperresponsiveness, remodeling, and smooth muscle mass: right answer, wrong reason?

Madavi N Oliver, Ben Fabry, Aleksandar Marinkovic, Srboljub M Mijailovich, James P Butler, Jeffrey J Fredberg

Open access · greenAbstract read
In one paragraph

Article in American journal of respiratory cell and molecular biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
7.6field-weighted citation impact, top 3% 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

51 citing papers in PubMed, 126 citations in OpenAlex.

  1. Article
  2. Review
  3. Airway smooth muscle function in asthma.Frontiers in physiology · 2022
    Review
  4. Article
  5. Structure and function of small airways in asthma patients revisited.European respiratory review : an official journal of the European Respiratory Society · 2021
    Review
  6. The Aftermath of Bronchoconstriction.Journal of engineering and science in medical diagnostics and therapy · 2019
    Review
  7. The Strain on Airway Smooth Muscle During a Deep Inspiration to Total Lung Capacity.Journal of engineering and science in medical diagnostics and therapy · 2019
    Article
  8. Review
  9. Review
  10. Article
  11. Transient stretch induces cytoskeletal fluidization through the severing action of cofilin.American journal of physiology. Lung cellular and molecular physiology · 2018
    Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

6 authors at 1 institution in 2 countries.

Madavi N OliverPhysiology Program, Department of Environmental Health, Harvard School of Public Health, Boston, Massachusetts, USA.
Ben Fabry
Aleksandar Marinkovic
Srboljub M Mijailovich
James P Butler
Jeffrey J Fredberg
Harvard University · US

Funding

RESISTANCE OF THE CELL TO SHAPE DISTORTION--BASIS OF CYTOSKELETAL MECHANICSP01HL033009 · NHLBI · HARVARD UNIVERSITY (SCH OF PUBLIC HLTH) · PI ROGERS, RICK · 1985 to 2005
$10.0M
AIRWAY MECHANICS AND SMOOTH MUSCLE SHORTENINGR01HL059682 · NHLBI · HARVARD UNIVERSITY (SCH OF PUBLIC HLTH) · PI FREDBERG, JEFFREY J · 1998 to 2006
$2.7M
NHLBI NIH HHS HL-33009NHLBI NIH HHS HL-59682
6 · The paper itself

Abstract

We quantified the effects of airway wall remodeling upon airway smooth muscle (ASM) shortening. Isolated ASM from sheep was attached to a servo-controller that applied a physiologic load. This load could be altered to reflect specified changes of airway wall geometry, elasticity, parenchymal tethering, transpulmonary pressure (P(L)), and fluctuations in P(L) associated with breathing. Starting at a reference length (L(ref)), ASM was stimulated with acetlycholine and held at constant P(L) of 4 cm H(2)O for 2 h. When all compartments were thickened to simulate the asthmatic airway but P(L) was held fixed, ASM shortened much more than that in the normal airway (to 0.52 L(ref) versus 0.66 L(ref)). When breathing with deep inspirations (DIs) was initiated, within the first three DIs the ASM in the normal airway lengthened to 0.84 L(ref), whereas that in the asthmatic airway remained stuck at 0.53 L(ref). Thickening of the smooth muscle layer alone produced the greatest muscle shortening (to 0.47 L(ref)) when compared with thickening of only submucosal (to 0.67 L(ref)) or only adventitial (to 0.62 L(ref)) compartments. With increased ASM mass, the ASM failed to lengthen in response to DIs, whereas in the airway with thickened submucosal and adventitial layers ASM lengthened dramatically (to 0.83 L(ref)). These findings confirm the long-held conclusion that increased muscle mass is the functionally dominant derangement, but mechanisms accounting for this conclusion differ dramatically from those previously presumed. Furthermore, increased ASM mass explained both hyperresponsiveness and the failure of a DI to relax the asthmatic airway.

Indexed as

Respiratory MechanicsAirway ResistanceAnimalsAsthmaHumansIn Vitro TechniquesModels, BiologicalMuscle ContractionMuscle, SmoothRespiratory HypersensitivitySheepTrachea

Identifiers

PMID17463392
PMCPMC1994228
OpenAlexW2134312563

What OpenQuestion holds

Textmetadata
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.