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Journal ArticleDOI

Mechanisms of Airway Remodeling

Nobuaki Hirota, +1 more
- 01 Sep 2013 - 
- Vol. 144, Iss: 3, pp 1026-1032
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TLDR
Airway remodeling is often considered the result of longstanding airway inflammation, but it may be present to an equivalent degree in the airways of children with asthma, raising the necessity for early and specific therapeutic interventions.
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This article is published in Chest.The article was published on 2013-09-01. It has received 260 citations till now. The article focuses on the topics: Airway.

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Citations
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Journal ArticleDOI

Triptolide inhibits transforming growth factor-β1-induced proliferation and migration of rat airway smooth muscle cells by suppressing nuclear factor-κB but not extracellular signal-regulated kinase 1/2

TL;DR: Triptolide may function as an inhibitor of asthma airway remodelling by suppressing ASMC proliferation and migration through inactivation of the NF‐κB pathway.
Journal ArticleDOI

Human airway smooth muscle cell proliferation from asthmatics is negatively regulated by semaphorin3A.

TL;DR: It is reported that semaphorin 3A (Sema3A) receptor, neuropilin 1 (Nrp1), is expressed on human ASM cells isolated from healthy and asthmatic donors and treatment of these cells with exogenous Sema 3A inhibits growth factor-induced proliferation.
Journal ArticleDOI

Smooth muscle brain-derived neurotrophic factor contributes to airway hyperreactivity in a mouse model of allergic asthma.

TL;DR: Novel data indicate that TrkB signaling is a key modulator of AHR and that smooth muscle‐derived BDNF mediates these effects during allergic airway inflammation and that Smooth muscle brain‐derived neurotrophic factor contributes to airway hyperreactivity in a mouse model of allergic asthma.
Journal ArticleDOI

Triptolide suppresses airway goblet cell hyperplasia and Muc5ac expression via NF-κB in a murine model of asthma.

TL;DR: Triptolide may inhibit airway goblet cell hyperplasia and Muc5ac expression in asthmatic mice via NF-κB and may be a potential drug for the treatment of patients with severe asthma.
References
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Journal ArticleDOI

Mepolizumab and Exacerbations of Refractory Eosinophilic Asthma

TL;DR: The results of this study suggest that eosinophils have a role as important effector cells in the pathogenesis of severe exacerbations of asthma in this patient population.
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Asthma exacerbations and sputum eosinophil counts: a randomised controlled trial.

TL;DR: A treatment strategy directed at normalisation of the induced sputum eosinophil count reduces asthma exacerbations and admissions without the need for additional anti-inflammatory treatment.
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Evidence That Severe Asthma Can Be Divided Pathologically into Two Inflammatory Subtypes with Distinct Physiologic and Clinical Characteristics

TL;DR: The results suggest that two distinct pathologic, physiologic, and clinical subtypes of severe asthma exist, with implications for further research and treatment.
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The relations between structural changes in small airways and pulmonary-function tests.

TL;DR: Pulmonary-function tests showed abnormalities at a time when the pathologic changes were still potentially reversible and when other tests were not appreciably changed, and increase in disease in small airways correlated with deterioration in lung function.
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