Autophagy in chronic obstructive pulmonary disease: Homeostatic or pathogenic mechanism?

Stefan W. Ryter, Zhi Hua Chen, Pyo Kim Hong, Augustine M.K. Choi

Research output: Contribution to journalArticle

54 Scopus citations

Abstract

Autophagy serves a critical function in cellular homeostasis by prolonging survival during nutrient deprivation. Although primarily characterized as a cell survival mechanism, the relationship between autophagy and cell death pathways remains incompletely understood. Autophagy heretofore has not been studied in the context of human pulmonary disease. We have recently observed increased morphological and biochemical markers of autophagy in human lung tissue from patients with chronic obstructive pulmonary disease (COPD). Similar observations of increased autophagy were also made in mouse lung tissue subjected to chronic cigarette smoke exposure, a primary causative agent in COPD, and in pulmonary cells exposed to aqueous cigarette smoke extract. Since knockdown of autophagic regulator proteins inhibited apoptosis in response to cigarette smoke exposure in vitro, we concluded that increased autophagy was associated with increased cell death in this model. We hypothesize that increased autophagy contributes to COPD pathogenesis by promoting epithelial cell death. Further research will examine whether autophagy plays a causative, correlative, or protective role in specific lung pathologies.

Original languageEnglish (US)
Pages (from-to)235-237
Number of pages3
JournalAutophagy
Volume5
Issue number2
DOIs
StatePublished - Feb 16 2009

Keywords

  • Apoptosis
  • Autophagy
  • Chronic obstructive pulmonary disease
  • Early growth response-1
  • Microtubule associated protein-1 light chain 3B

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology

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