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

Juan Shi; Hui Li; Chao Yuan; Meihui Luo; Jun Wei; Xiaoming Liu

doi:10.1155/2018/6567578

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

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

Juan Shi, Hui Li, Chao Yuan, Meihui Luo, Jun Wei and Xiaoming Liu

Oxidative medicine and cellular longevity, Vol.2018, pp.6567578-13

04/23/2018

DOI: 10.1155/2018/6567578

PMCID: PMC5937428

PMID: 29849907

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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.

Details

Title: Subtitle: Cigarette Smoke-Induced Acquired Dysfunction of Cystic Fibrosis Transmembrane Conductance Regulator in the Pathogenesis of Chronic Obstructive Pulmonary Disease
Creators: Juan Shi - College of Clinical Medicine Ningxia Medical University Yinchuan Ningxia 750004 Chinanxmu.edu.cn
Hui Li - College of Clinical Medicine Ningxia Medical University Yinchuan Ningxia 750004 Chinanxmu.edu.cn
Chao Yuan - College of Life Science Ningxia University Yinchuan Ningxia 750021 Chinanxu.edu.cn
Meihui Luo - College of Clinical Medicine Ningxia Medical University Yinchuan Ningxia 750004 Chinanxmu.edu.cn
Jun Wei - College of Clinical Medicine Ningxia Medical University Yinchuan Ningxia 750004 Chinanxmu.edu.cn
Xiaoming Liu - College of Clinical Medicine Ningxia Medical University Yinchuan Ningxia 750004 Chinanxmu.edu.cn
Contributors: Kota V Ramana (Editor)
Resource Type: Journal article
Publication Details: Oxidative medicine and cellular longevity, Vol.2018, pp.6567578-13
DOI: 10.1155/2018/6567578
PMID: 29849907
PMCID: PMC5937428
NLM abbreviation: Oxid Med Cell Longev
ISSN: 1942-0900
eISSN: 1942-0994
Publisher: Hindawi
Grant note: 81460247; 31472191 / National Natural Science Foundation of China
Language: English
Date published: 04/23/2018
Academic Unit: Anatomy and Cell Biology; Pathology
Record Identifier: 9984025362602771

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