scholarly journals Augmentation of S-Nitrosoglutathione Controls Cigarette Smoke-Induced Inflammatory–Oxidative Stress and Chronic Obstructive Pulmonary Disease-Emphysema Pathogenesis by Restoring Cystic Fibrosis Transmembrane Conductance Regulator Function

2017 ◽  
Vol 27 (7) ◽  
pp. 433-451 ◽  
Author(s):  
Manish Bodas ◽  
David Silverberg ◽  
Kyla Walworth ◽  
Kathryn Brucia ◽  
Neeraj Vij
Keyword(s):  
Oxidative Stress ◽  
Chronic Obstructive Pulmonary Disease ◽  
Cystic Fibrosis ◽  
Pulmonary Disease ◽  
Cigarette Smoke ◽  
Chronic Obstructive ◽  
Transmembrane Conductance Regulator ◽  
Transmembrane Conductance ◽  
Obstructive Pulmonary Disease ◽  
Cystic Fibrosis Transmembrane

scholarly journals Cigarette Smoke-Induced Acquired Dysfunction of Cystic Fibrosis Transmembrane Conductance Regulator in the Pathogenesis of Chronic Obstructive Pulmonary Disease

2018 ◽  
Vol 2018 ◽  
pp. 1-13 ◽  
Author(s):  
Juan Shi ◽  
Hui Li ◽  
Chao Yuan ◽  
Meihui Luo ◽  
Jun Wei ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Chronic Obstructive Pulmonary Disease ◽  
Cystic Fibrosis ◽  
Pulmonary Disease ◽  
Cigarette Smoke ◽  
Chronic Obstructive ◽  
Transmembrane Conductance Regulator ◽  
Transmembrane Conductance ◽  
Obstructive Pulmonary Disease ◽  
Cystic Fibrosis Transmembrane

Chronic obstructive pulmonary disease (COPD) is a disease state characterized by airflow limitation that is not fully reversible. Cigarette smoke and oxidative stress are main etiological risks in COPD. Interestingly, recent studies suggest a considerable overlap between chronic bronchitis (CB) phenotypic COPD and cystic fibrosis (CF), a common fatal hereditary lung disease caused by genetic mutations of the cystic fibrosis transmembrane conductance regulator (CFTR) gene. Phenotypically, CF and COPD are associated with an impaired mucociliary clearance and mucus hypersecretion, although they are two distinct entities of unrelated origin. Mechanistically, the cigarette smoke-increased oxidative stress-induced CFTR dysfunction is implicated in COPD. This underscores CFTR in understanding and improving therapies for COPD by altering CFTR function with antioxidant agents and CFTR modulators as a great promising strategy for COPD treatments. Indeed, treatments that restore CFTR function, including mucolytic therapy, antioxidant ROS scavenger, CFTR stimulator (roflumilast), and CFTR potentiator (ivacaftor), have been tested in COPD. This review article is aimed at summarizing the molecular, cellular, and clinical evidence of oxidative stress, particularly the cigarette smoke-increased oxidative stress-impaired CFTR function, as well as signaling pathways of CFTR involved in the pathogenesis of COPD, with a highlight on the therapeutic potential of targeting CFTR for COPD treatment.

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