Phenotype modulation of airway smooth muscle in asthma

Wright, Donna; Trian, Thomas; Siddiqui, Sana; Pascoe, Chris D.; Johnson, Jill; Dekkers, Bart G. J.; Dakshinamurti, Shyamala; Bagchi, Rushita A.; Burgess, Janette K.; Kanabar, Varsha; Ojo, Oluwaseun O.

doi:10.1016/j.pupt.2012.08.005

Cited by 84 publications

(80 citation statements)

References 93 publications

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“…This evidence argues that the enhanced contractility would be acquired because of the exposure to inflammatory cytokines, and the contribution of this molecular pathway in the development of asthmatic AHR would reflect the intrinsic difference of asthmatic ASM cells that fosters a greater CD38 upregulation in response to cytokine exposure. This finding supports current growing evidence describing phenotypic changes in ASM between healthy and asthmatic subjects [5]. Accordingly, J.…”

Section: Acquired Hypercontractilitysupporting

confidence: 91%

Smooth Muscle Hypercontractility in Airway Hyperresponsiveness: Innate, Acquired, or Nonexistent?

et al. 2013

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Section: Acquired Hypercontractilitysupporting

confidence: 91%

Smooth Muscle Hypercontractility in Airway Hyperresponsiveness: Innate, Acquired, or Nonexistent?

et al. 2013

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“…Alternatively, the inflammatory milieu may induce the transition of asthmatic ASM from a contractile to a “synthetic” phenotype (reviewed in (76)). This synthetic ASM phenotype is characterised by reduced contractile-associated proteins but increased proliferation and chemokine secretion.…”

Section: Mechanisms Of Airway Hyperresponsivenessmentioning

confidence: 99%

Mechanisms of airway hyper‐responsiveness in asthma: the past, present and yet to come

Chapman

Irvin

2015

Clin Experimental Allergy

120

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Airway hyperresponsiveness (AHR) has long been considered a cardinal feature of asthma. The development of the measurement of AHR forty years ago initiated many important contributions to our understanding of asthma and other airway diseases. However, our understanding of AHR in asthma remains complicated by the multitude of potential underlying mechanisms which in reality are likely to have different contributions amongst individual patients. Therefore the present review will discuss the current state of understanding of the major mechanisms proposed to contribute to AHR and highlight the way in which AHR testing is beginning to highlight distinct abnormalities associated with clinically relevant patient populations. In doing so we aim to provide a foundation by which future research can begin to ascribe certain mechanisms to specific patterns of bronchoconstriction and subsequently match phenotypes of bronchoconstriction with clinical phenotypes. We believe that this approach is not only within our grasp but will lead to improved mechanistic understanding of asthma phenotypes and hopefully better inform the development of phenotype-targeted therapy.

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“…Airway smooth muscle cells have the ability to change the degree of various functions, such as contractility, proliferation, migration, and synthesis of inflammatory mediators Halayko et al, 2008;Wright et al, 2013). The plasticity from a contractile phenotype to other phenotypes (proliferation, migration, or secretion of chemical mediators) may enhance airway inflammation, leading to airway remodeling, which is also characteristic of asthma and COPD.…”

Section: Possible Effects Of Bronchodilators On Airway Inflammationmentioning

confidence: 99%

Research and development of bronchodilators for asthma and COPD with a focus on G protein/KCa channel linkage and β2-adrenergic intrinsic efficacy

Kumakura

Fukunaga

Oguma

2015

Pharmacology & Therapeutics

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Phenotype modulation of airway smooth muscle in asthma

Cited by 84 publications

References 93 publications

Smooth Muscle Hypercontractility in Airway Hyperresponsiveness: Innate, Acquired, or Nonexistent?

Smooth Muscle Hypercontractility in Airway Hyperresponsiveness: Innate, Acquired, or Nonexistent?

Mechanisms of airway hyper‐responsiveness in asthma: the past, present and yet to come

Research and development of bronchodilators for asthma and COPD with a focus on G protein/KCa channel linkage and β2-adrenergic intrinsic efficacy

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