Autophagy in the lung. Review uri icon

Overview

MeSH

  • Animals
  • Anoxia
  • Apoptosis
  • Early Growth Response Protein 1
  • Homeostasis
  • Humans
  • Inflammation
  • Lung Neoplasms
  • Lysosomes
  • Mice
  • Oxidative Stress
  • Starvation

MeSH Major

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

abstract

  • Autophagy is a cellular process for the disposal of damaged organelles or denatured proteins through a lysosomal degradation pathway. By reducing endogenous macromolecules to their basic components (i.e., amino acids, lipids), autophagy serves a homeostatic function by ensuring cell survival during starvation. Increased autophagy can be found in dying cells, although the relationships between autophagy and programmed cell death remain unclear. To date, few studies have examined the regulation and functional significance of autophagy in human lung disease. The lung, a complex organ that functions primarily in gas exchange, consists of diverse cell types (i.e., endothelial, epithelial, mesenchymal, inflammatory). In lung cells, autophagy may represent a general inducible adaptive response to injury resulting from exposure to stress agents, including hypoxia, oxidants, inflammation, ischemia-reperfusion, endoplasmic reticulum stress, pharmaceuticals, or inhaled xenobiotics (i.e., air pollution, cigarette smoke). In recent studies, we have observed increased autophagy in mouse lungs subjected to chronic cigarette smoke exposure, and in pulmonary epithelial cells exposed to cigarette smoke extract. Knockdown of autophagic proteins inhibited apoptosis in response to cigarette smoke exposure in vitro, suggesting that increased autophagy was associated with epithelial cell death. We have also observed increased morphological and biochemical markers of autophagy in human lung specimens from patients with chronic obstructive pulmonary disease (COPD). We hypothesize that increased autophagy contributes to COPD pathogenesis by promoting epithelial cell death. Further research will examine whether autophagy plays a homeostatic or maladaptive role in COPD and other human lung diseases.

publication date

  • February 2010

has subject area

  • Animals
  • Anoxia
  • Apoptosis
  • Autophagy
  • Early Growth Response Protein 1
  • Homeostasis
  • Humans
  • Inflammation
  • Lung
  • Lung Neoplasms
  • Lysosomes
  • Mice
  • Oxidative Stress
  • Pulmonary Disease, Chronic Obstructive
  • Smoking
  • Starvation

Research

keywords

  • Journal Article
  • Review

Identity

Language

  • eng

PubMed Central ID

  • PMC3137145

Digital Object Identifier (DOI)

  • 10.1513/pats.200909-101JS

PubMed ID

  • 20160144

Additional Document Info

start page

  • 13

end page

  • 21

volume

  • 7

number

  • 1