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Cited by 42Asthma and respiratory diseasesCellular Mechanics and InteractionsMuscle Physiology and Disorders

The DOI matches its Crossref record.

Disrupting actin–myosin–actin connectivity in airway smooth muscle as a treatment for asthma?

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Lavoie, Tera L., Dowell, Maria L., Lakser, Oren J., Gerthoffer, William T., Fredberg, Jeffrey J., Seow, Chun Y., Mitchell, Richard W., Solway, Julian·2009·Proceedings of the American Thoracic Society
DOI 10.1513/pats.200808-078rmPMC PMC2677405
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Abstract

Breathing is known to functionally antagonize bronchoconstriction caused by airway muscle contraction. During breathing, tidal lung inflation generates force fluctuations that are transmitted to the contracted airway muscle. In vitro, experimental application of force fluctuations to contracted airway smooth muscle strips causes them to relengthen. Such force fluctuation–induced relengthening (FFIR) likely represents the mechanism by which breathing antagonizes bronchoconstriction. Thus, understanding the mechanisms that regulate FFIR of contracted airway muscle could suggest novel therapeutic interventions to increase FFIR, and so to enhance the beneficial effects of breathing in suppressing bronchoconstriction. Here we propose that the connectivity between actin filaments in contracting airway myocytes is a key determinant of FFIR, and suggest that disrupting actin-myosin-actin connectivity by interfering with actin polymerization or with myosin polymerization merits further evaluation as a potential novel approach for preventing prolonged bronchoconstriction in asthma.

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  • Intermittent deep breaths have been shown to be functional in reducing airway resistance, probably by re-lengthening the contracted smooth muscles of the airways.

    “Intermittent deep breaths have been shown to be functional in reducing airway resistance, probably by re-lengthening the contracted smooth muscles of the airways (Lavoie et al., 2009).”

    From The psychophysiology of blood-injection-injury phobia: Looking beyond the diphasic response paradigm (2010) · cites this paper as Lavoie et al., 2009

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Metadata

Authors
Lavoie, T. L., Dowell, M. L., Lakser, O. J., Gerthoffer, W. T., Fredberg, J. J., Seow, C. Y., Mitchell, R. W., & Solway, J.
Affiliations
  • University of Chicago (US)
  • University of South Alabama (US)
  • Harvard University (US)
  • University of British Columbia (CA)
ORCID
Venue
Proceedings of the American Thoracic Society
Publisher
Oxford University Press (OUP)
Published
2009-05-01
Volume
6
Issue
3
Pages
295-300
ISSN
  • 1546-3222 (ISSN-L)
  • 1943-5665
DOI
10.1513/pats.200808-078rm
PMC
PMC2677405
OpenAlex
W2054992221
Cited by
42
References
0
Citations by year
2025: 2 · 2024: 2 · 2023: 1 · 2022: 1 · 2021: 1 · 2020: 3 · 2019: 4 · 2018: 2 · 2017: 2 · 2016: 2 · 2015: 2 · 2014: 4 · 2013: 4 · 2012: 4
FWCI
0.57
Type
journal article
Language
en
Open access
Licence
academic.oup.com/pages/standard-publication-reuse-rights (vor)
Locations
  • Proceedings of the American Thoracic Society (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health
  • National Heart, Lung, and Blood Institute (HL007605, R01HL079398, K08HL086604)
Topics
  • Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Asthma and respiratory diseases
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Cellular Mechanics and Interactions
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
Keywords
asthma, airway smooth muscle, bronchoconstriction, actin polymerization, breathing, therapeutic target
MeSH terms
Asthma, Humans, Actin Cytoskeleton, Bronchoconstriction, Smooth Muscle Myosins

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