Airway Remodeling from Bench to Bedside: Current Perspectives

Slade, David; Kraft, Monica

doi:10.1016/j.ccm.2005.11.001

Cited by 19 publications

(12 citation statements)

References 153 publications

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“…[10][11][12] Structural changes seen in asthmatic patients can include thickening of the airway wall reticular basement membrane, formation of an abnormal elastic fiber network, alterations in airway cartilage structure, angiogenesis, and increase in airway smooth muscle mass. [13][14][15] Tissue collagen deposition is known to be controlled by 2 classes of molecules: matrix metalloproteinases (MMPs), which degrade collagen, and tissue inhibitors of metalloproteinases (TIMPs). 14,16 Studies of asthmatic patients demonstrate increased production of both MMP-9 and TIMP-1 by alveolar macrophages and increased quantities of these mediators in the sputum, bronchoalveolar lavage (BAL) fluid, and biopsy specimens.…”

mentioning

confidence: 99%

Airway remodeling and lack of bronchodilator response in steroid-resistant asthma

Goleva

Hauk

Boguniewicz

et al. 2007

Journal of Allergy and Clinical Immunology

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mentioning

confidence: 99%

Airway remodeling and lack of bronchodilator response in steroid-resistant asthma

Goleva

Hauk

Boguniewicz

et al. 2007

Journal of Allergy and Clinical Immunology

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“…ASMC contribute significantly to airway remodeling and release proinflammatory cytokines, thereby recruiting more immune cells into the inflamed airway (6,17,45).…”

mentioning

confidence: 99%

Dimethylfumarate inhibits NF-κB function at multiple levels to limit airway smooth muscle cell cytokine secretion

Seidel

Merfort²,

Hughes³

et al. 2009

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…Data exist suggesting that epithelial damage participates in the pro-inflammatory process by releasing cytokines, growth factors, and mediators (40,52). Epithelial damage induces up-regulation of receptors, specifically members of the EGFR family that drive proliferation and repair.…”

Section: Epithelial-mesenchymal Unitmentioning

confidence: 99%

“…Collagen, reticular and elastic fibers, proteoglycans and glycoproteins, all of which contribute to lung remodeling, can be produced by mesenchymal cells influenced by epithelial cells. Thus, epithelial-mesenchymal interactions play an important role in extracellular matrix production and deposition (52,53). Furthermore, the Th2-type cytokines IL-4 and IL-13, signaling via the transcription factor STAT-6, are able to induce myofibroblast transformation and submucosal remodeling through a TGF-ß-depending mechanism.…”

Section: Epithelial-mesenchymal Unitmentioning

confidence: 99%

“…Actually, remodeling can be defined as structural changes during growth or in response to injury or inflammation. Airway remodeling is not an inherently abnormal response, but either an appropriate step in normal lung development or repair, or a series of events that can lead to pathophysiological consequences (52). Communication between the epithelium and the fibroblast sheet is reminiscent of the morphogenesis process during which epithelium and mesenchyme form a trophic unit (56).…”

Section: Epithelial-mesenchymal Unitmentioning

confidence: 99%

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Asthma: where is it going?

Faffe¹

2008

Braz J Med Biol Res

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Asthma is characterized by reversible airway obstruction, airway hyperresponsiveness, and airway inflammation. Although our understanding of its pathophysiological mechanisms continues to evolve, the relative contributions of airway hyperresponsiveness and inflammation are still debated. The first mechanism identified as important for asthma was bronchial hyperresponsiveness. In a second step, asthma was recognized also as an inflammatory disease, with chronic inflammation inducing structural changes or remodeling. However, persistence of airway dysfunction despite inflammatory control is observed in chronic severe asthma of both adults and children. More recently, a potential role for epithelial-mesenchymal communication or transition is emerging, with epithelial injury often resulting in a self-sustaining phenotype of wound repair modulation by activation/ reactivation of the epithelial-mesenchymal trophic unit, suggesting that chronic asthma can be more than an inflammatory disease. It is noteworthy that the gene-environmental interactions critical for the development of a full asthma phenotype involve processes similar to those occurring in branching morphogenesis. In addition, a central role for airway smooth muscle in the pathogenesis of the disease has been explored, highlighting its secretory function as well as different intrinsic properties compared to normal subjects. These new concepts can potentially shed light on the mechanisms underlying some asthma phenotypes and improve our understanding of the disease in terms of the therapeutic strategies to be applied. How we understand asthma and its mechanisms along time will be the focus of this overview.

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Airway Remodeling from Bench to Bedside: Current Perspectives

Cited by 19 publications

References 153 publications

Airway remodeling and lack of bronchodilator response in steroid-resistant asthma

Airway remodeling and lack of bronchodilator response in steroid-resistant asthma

Dimethylfumarate inhibits NF-κB function at multiple levels to limit airway smooth muscle cell cytokine secretion

Asthma: where is it going?

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