Autophagy in cigarette smoke-induced chronic obstructive pulmonary disease. Review uri icon

Overview

MeSH

  • Animals
  • Apoptosis
  • Humans
  • Signal Transduction

MeSH Major

  • Autophagy
  • Lung
  • Pulmonary Disease, Chronic Obstructive
  • Smoking

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.

publication date

  • October 2010

has subject area

  • Animals
  • Apoptosis
  • Autophagy
  • Humans
  • Lung
  • Pulmonary Disease, Chronic Obstructive
  • Signal Transduction
  • Smoking

Research

keywords

  • Journal Article
  • Review

Identity

Language

  • eng

PubMed Central ID

  • PMC3081520

Digital Object Identifier (DOI)

  • 10.1586/ers.10.61

PubMed ID

  • 20923337

Additional Document Info

start page

  • 573

end page

  • 584

volume

  • 4

number

  • 5