Autophagy in cigarette smoke-induced chronic obstructive pulmonary disease

Stefan W. Ryter, Seon Jin Lee, Augustine M.K. Choi

Research output: Contribution to journalReview article

53 Scopus citations

Abstract

The molecular and cellular mechanisms underlying the pathogenesis of chronic obstructive pulmonary disease (COPD) remain incompletely understood. We have investigated the potential role of macro-autophagy, a cellular homeostatic mechanism, in COPD and cigarette smoke-induced lung-cell injury. Autophagy is a dynamic process for the turnover of organelles and proteins, which regenerates metabolic precursors through the lysosomal-dependent catabolism of cellular macromolecules. It is typically associated with survival pathways, especially in nutrient deficiency states. The role of autophagy in human diseases is less clear, and has been associated with both protective and detrimental consequences, depending on the disease model. While autophagy is considered cytoprotective, this process is often found in association with cell death, and the relationships between autophagy and cell death remain ambiguous. We have found elevated autophagy in COPD lung specimens, as well as in response to cigarette smoke exposure in vitro and in vivo. In our studies, the activation of autophagic proteins was associated with epithelial cell apoptosis in response to cigarette smoke, with pathogenic implications in COPD. Further studies are needed to determine the functional significance of autophagy in COPD and other diseases of the lung.

Original languageEnglish (US)
Pages (from-to)573-584
Number of pages12
JournalExpert Review of Respiratory Medicine
Volume4
Issue number5
DOIs
StatePublished - Oct 2010

Keywords

  • apoptosis
  • autophagy
  • chronic obstructive pulmonary disease
  • cigarette smoke
  • emphysema

ASJC Scopus subject areas

  • Immunology and Allergy
  • Pulmonary and Respiratory Medicine
  • Public Health, Environmental and Occupational Health

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