Chronic obstructive pulmonary disease and the modulation of CFTR by acute exposure to cigarette smoke

Chronic obstructive pulmonary disease (COPD) is a leading cause of death and cigarette smoke is the main risk factor. Detecting its earliest stages and preventing a decline in lung function are key goals. The pathogenesis of COPD is complex but has some similarities to cystic fibrosis (CF), a disease caused by mutations in the cftr gene. CF leads to chronic inflammation, abnormal mucus, and cycles of infection. Cigarette smoke exposure also causes CFTR dysfunction, and it is probably not a coincidence that inflammation, mucus obstruction, and infections are also characteristics of COPD, although the exacerbations can be quite different. We review here the acute effects of cigarette smoke on CFTR function and its potential role in COPD. Understanding CFTR regulation by cigarette smoke may identify novel drug targets and facilitate the development of therapeutics that reduce the progression and severity of COPD.

Automated summary

Chronic obstructive pulmonary disease (COPD) is a leading cause of death, with cigarette smoke being the main risk factor. COPD shares similarities with cystic fibrosis (CF), particularly in terms of inflammation, mucus obstruction, and infection. Understanding the effects of cigarette smoke on CFTR function may lead to the development of novel therapeutics for reducing the progression and severity of COPD.