Molecular processes that drive cigarette smoke-induced epithelial cell fate of the lung

Am J Respir Cell Mol Biol. 2014 Mar;50(3):471-82. doi: 10.1165/rcmb.2013-0348TR.


Cigarette smoke contains numerous chemical compounds, including abundant reactive oxygen/nitrogen species and aldehydes, and many other carcinogens. Long-term cigarette smoking significantly increases the risk of various lung diseases, including chronic obstructive pulmonary disease and lung cancer, and contributes to premature death. Many in vitro and in vivo studies have elucidated mechanisms involved in cigarette smoke-induced inflammation, DNA damage, and autophagy, and the subsequent cell fates, including cell death, cellular senescence, and transformation. In this Translational Review, we summarize the known pathways underlying these processes in airway epithelial cells to help reveal future challenges and describe possible directions of research that could lead to better management and treatment of these diseases.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Cell Death
  • Cellular Senescence
  • DNA Damage
  • Epithelial Cells / drug effects*
  • Epithelial Cells / metabolism
  • Epithelial Cells / pathology
  • Humans
  • Inflammation Mediators / metabolism
  • Lung Diseases / etiology*
  • Lung Diseases / metabolism
  • Lung Diseases / pathology
  • Prognosis
  • Respiratory Mucosa / drug effects*
  • Respiratory Mucosa / metabolism
  • Respiratory Mucosa / pathology
  • Risk Factors
  • Signal Transduction / drug effects
  • Smoke / adverse effects*
  • Smoking / adverse effects*


  • Inflammation Mediators
  • Smoke