Journal ArticleDOI
Mechanisms of Airway Remodeling
Nobuaki Hirota,James G. Martin +1 more
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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.About:
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.read more
Citations
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Journal ArticleDOI
TGF-β1 Signaling and Tissue Fibrosis.
TL;DR: The current understanding of the core functions of TGF-β1 in promoting collagen accumulation, parallel pathways that promote physiological repair, and pathological triggers that tip the balance toward progressive fibrosis are examined.
Journal ArticleDOI
Oxidative stress-induced mitochondrial dysfunction drives inflammation and airway smooth muscle remodeling in patients with chronic obstructive pulmonary disease.
Coen Wiegman,Charalambos Michaeloudes,Gulammehdi Haji,Priyanka Narang,Colin Clarke,Kirsty E. Russell,Wuping Bao,Stelios Pavlidis,Peter J. Barnes,Justin Kanerva,Anton Bittner,Navin Rao,Michael P. Murphy,Paul Kirkham,Kian Fan Chung,Ian M. Adcock,Christopher E. Brightling,Donna E. Davies,Donna K. Finch,Andrew J. Fisher,Alasdair Gaw,Alan J. Knox,Ruth J. Mayer,Michael I. Polkey,Michael Salmon,David Singh +25 more
TL;DR: Mitochondrial dysfunction in patients with COPD is associated with excessive mitochondrial ROS levels, which contribute to enhanced inflammation and cell hyperproliferation.
Journal ArticleDOI
Neutrophilic Inflammation in Asthma and Association with Disease Severity.
Anuradha Ray,Jay K. Kolls +1 more
TL;DR: Current knowledge of the role of neutrophils in asthma is reviewed and future avenues of research in this field are highlighted to help delineate different subtypes of asthma.
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Cellular and molecular mechanisms of asthma and COPD.
TL;DR: The inflammatory and cellular mechanisms of asthma and COPD are compared and the differences in inflammatory cells and profile of inflammatory mediators are highlighted to better understand the underlying cellular and molecular mechanisms in order to develop new treatments in areas of unmet need.
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Airway remodeling in asthma: what really matters.
TL;DR: This review will address a few major aspects: what are reliable quantitative approaches to assess airway remodeling, and are there any indications supporting the notion that airways remodeling can occur as a primary event, i.e., before any inflammatory process was initiated?
References
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MCP-1/CCR2B-dependent loop upregulates MUC5AC and MUC5B in human airway epithelium.
TL;DR: Treatment approaches targeting MCP-1/CCR2B may be useful in preventing not only influx of inflammatory cells to the airways but also mucus hypersecretion and goblet cell hyperplasia.
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Bronchial vascular remodelling in patients with COPD and its relationship with inhaled steroid treatment.
Andrea Zanini,Alfredo Chetta,Marina Saetta,Simonetta Baraldo,Claudia Castagnetti,Gabriele Nicolini,Margherita Neri,Dario Olivieri +7 more
TL;DR: Bronchial vascular remodelling in patients with COPD is mainly related to morphological changes of the mucosal microvessels rather than to new vessel formation, and may be reduced in patients treated with steroids.
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In vivo imaging of the airway wall in asthma: fibered confocal fluorescence microscopy in relation to histology and lung function
TL;DR: The association between post-bronchodilator FEV1 %predicted and both histological and FCFM elastic fibre patterns points towards a structure-function relationship between extracellular matrix in the airway wall and lung function.
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TNF-α–Converting Enzyme/A Disintegrin and Metalloprotease−17 Mediates Mechanotransduction in Murine Tracheal Epithelial Cells
Tetsuya Shiomi,Daniel J. Tschumperlin,Jin-Ah Park,Susan W. Sunnarborg,Keisuke Horiuchi,Carl P. Blobel,Jeffrey M. Drazen +6 more
TL;DR: The data provide strong evidence that TACE plays a critical central role in the transduction of compressive stress and a pivotal role for proteolytic EGF-family ligand shedding.