Stress oxydatif, tabagisme et CFTR

Ouellet, Cristine; Bilodeau, Ginette; Cantin, André M.

doi:10.1051/medsci/20072319

Cited by 2 publications

(1 citation statement)

References 10 publications

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“…Additionally, the question of whether ENaC regulates CFTR activity remains unclear (46). Furthermore, understanding the mechanism of the ENaC-CFTR cross talk in airway epithelia is complicated by the fact that CFTR activity and ENaC function are often affected by the same physiological [␤-agonists (7,179)] and environmental factors that include oxidative stress (19,20,175,203,218,248), hypoxia (36,244), inflammatory responses (28,30,169,202,241), and influenza infections (102,109,144,189,235).…”

Section: Chloride Transportmentioning

confidence: 99%

Ion channels of the lung and their role in disease pathogenesis

Bartoszewski

Matalon

Collawn

2017

American Journal of Physiology-Lung Cellular and Molecular Phys

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Maintenance of normal epithelial ion and water transport in the lungs includes providing a thin layer of surface liquid that coats the conducting airways. This airway surface liquid is critical for normal lung function in a number of ways but, perhaps most importantly, is required for normal mucociliary clearance and bacterial removal. Preservation of the appropriate level of hydration, pH, and viscosity for the airway surface liquid requires the proper regulation and function of a battery of different types of ion channels and transporters. Here we discuss how alterations in ion channel/transporter function often lead to lung pathologies.

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Section: Chloride Transportmentioning

confidence: 99%

Ion channels of the lung and their role in disease pathogenesis

Bartoszewski

Matalon

Collawn

2017

American Journal of Physiology-Lung Cellular and Molecular Phys

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Inflammation in cystic fibrosis lung disease: Pathogenesis and therapy

Cantin

Hartl

Konstan

et al. 2015

Journal of Cystic Fibrosis

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378

322

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Lung disease is the major cause of morbidity and mortality in patients with cystic fibrosis (CF). Although CF lung disease is primarily an infectious disorder, the associated inflammation is both intense and ineffective at clearing pathogens. Persistent high-intensity inflammation leads to permanent structural damage of the CF airways and impaired lung function that eventually results in respiratory failure and death. Several defective inflammatory responses have been linked to cystic fibrosis transmembrane conductance regulator (CFTR) deficiency including innate and acquired immunity dysregulation, cell membrane lipid abnormalities, various transcription factor signaling defects, as well as altered kinase and toll-like receptor responses. The inflammation of the CF lung is dominated by neutrophils that release oxidants and proteases, particularly elastase. Neutrophil elastase in the CF airway secretions precedes the appearance of bronchiectasis, and correlates with lung function deterioration and respiratory exacerbations. Anti-inflammatory therapies are therefore of particular interest for CF lung disease but must be carefully studied to avoid suppressing critical elements of the inflammatory response and thus worsening infection. This review examines the role of inflammation in the pathogenesis of CF lung disease, summarizes the results of past clinical trials and explores promising new anti-inflammatory options.

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Stress oxydatif, tabagisme et CFTR

Cited by 2 publications

References 10 publications

Ion channels of the lung and their role in disease pathogenesis

Ion channels of the lung and their role in disease pathogenesis

Inflammation in cystic fibrosis lung disease: Pathogenesis and therapy

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