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.
Journal ArticleDOI
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.
Journal ArticleDOI
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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Journal ArticleDOI
Fluticasone inhibits but does not reverse allergen-induced structural airway changes.
TL;DR: It is concluded that concomitant treatment with FP partly inhibits structural airway changes as well as hyperresponsiveness induced by OA exposure, and post hoc treatment fails to reverse established airway remodeling.
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Cysteinyl leukotrienes promote human airway smooth muscle migration.
Krishnan Parameswaran,Gerard Cox,Katherine Radford,Luke J. Janssen,Roma Sehmi,Paul M. O'Byrne +5 more
TL;DR: It is suggested that cysteinyl leukotrienes play an augmentary role in human ASM migration and the phosphatidylinositol-3 kinase pathway is a key signaling mechanism in the chemotactic migration of ASM cells in response to cysteiny leukOTrienes.
Epithelial EGF receptor signaling mediates airway hyperreactivity and remodeling
Timothy D. Le Cras,Thomas H. Acciani,Elizabeth M. Mushaben,Elizabeth L. Kramer,Patricia A. Pastura,William D. Hardie,R. Korfhagen,Umasundari Sivaprasad,Mark B. Ericksen,Aaron,Michael J. Holtzman,Jeffrey A. Whitsett,Gurjit K. Khurana +12 more
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Mechanisms of induction of airway smooth muscle hyperplasia by transforming growth factor-β
TL;DR: It is suggested that TGF-beta1 may act in an autocrine fashion to induce ASM hyperplasia, mediated by its receptor and several kinases including PI3K, ERK, and JNK, whereas p38 MAPK is a negative regulator.
Journal ArticleDOI
Angiotensin receptor blockade attenuates cigarette smoke–induced lung injury and rescues lung architecture in mice
Megan Podowski,Carla L. Calvi,Shana Metzger,Kaori Misono,Hataya Poonyagariyagorn,Armando Lopez-Mercado,Therese Ku,Thomas Lauer,Sharon A. McGrath-Morrow,Alan E. Berger,Christopher Cheadle,Rubin M. Tuder,Rubin M. Tuder,Harry C. Dietz,Wayne Mitzner,Robert A. Wise,Enid Neptune +16 more
TL;DR: Data support the hypothesis that inhibition of TGF-β signaling through angiotensin receptor blockade can attenuate CS-induced lung injury in an established murine model, and provide a preclinical platform for the development of other T GF-β-targeted therapies for patients with COPD.