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Oxid Med Cell Longev. 2018 Apr 23;2018:6567578. doi: 10.1155/2018/6567578. eCollection 2018.

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

Shi J1,2, Li H1,2,3, Yuan C4, Luo M1,4, Wei J1,2,3, Liu X1,2,3,4.

Author information

1
College of Clinical Medicine, Ningxia Medical University, Yinchuan, Ningxia 750004, China.
2
Ningxia Key Laboratory of Clinical and Pathological Microbiology, General Hospital of Ningxia Medical University, Yinchuan, Ningxia 750004, China.
3
Ningxia Institute for Stem Cell Research, General Hospital of Ningxia Medical University, Yinchuan, Ningxia 750004, China.
4
College of Life Science, Ningxia University, Yinchuan, Ningxia 750021, China.

Abstract

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.

PMID:
29849907
PMCID:
PMC5937428
DOI:
10.1155/2018/6567578
[Indexed for MEDLINE]
Free PMC Article

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