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

Am J Physiol Cell Physiol. 2022 Nov 1;323(5):C1374-C1392. doi: 10.1152/ajpcell.00356.2022. Epub 2022 Sep 19.

Abstract

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.

Keywords: ROS; air pollution; chronic obstructive pulmonary disease; cigarette smoke; cystic fibrosis.

Publication types

  • Review
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cigarette Smoking* / adverse effects
  • Cystic Fibrosis Transmembrane Conductance Regulator / genetics
  • Cystic Fibrosis* / genetics
  • Humans
  • Inflammation
  • Nicotiana
  • Pulmonary Disease, Chronic Obstructive* / genetics

Substances

  • Cystic Fibrosis Transmembrane Conductance Regulator
  • CFTR protein, human

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