Autophagy in chronic lung disease

Prog Mol Biol Transl Sci. 2020:172:135-156. doi: 10.1016/bs.pmbts.2020.02.001. Epub 2020 Mar 12.

Abstract

The development of chronic lung disease occurs as a consequence of multiple cellular events that involve an initial insult which often leads to the development of chronic inflammation, and the dysregulation of cellular proliferation and cell death mechanisms. Multiple cell types in the lung are key to the respiratory and protective/barrier functions necessary to manage the chronic exposures to environmental, mechanical, and oxidative stressors. Autophagy is essential to lung development and homeostasis, as well as the prevention and development of disease. The cellular process involves the collection and removal of unwanted organelles and proteins through lysosomal degradation. In recent years, investigations have addressed the roles of autophagy and selective autophagy in numerous chronic lung diseases. Here, we highlight recent advances on the role of autophagy in the pathogenesis of asthma, chronic obstructive pulmonary disease and emphysema, pulmonary arterial hypertension, and idiopathic pulmonary fibrosis.

Keywords: Asthma; Autophagy; COPD; Emphysema; Idiopathic pulmonary fibrosis; Pulmonary hypertension.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Animals
  • Autophagosomes / physiology
  • Autophagy*
  • Cigarette Smoking / pathology
  • Disease Models, Animal
  • Homeostasis
  • Humans
  • Inflammation / pathology
  • Lung / growth & development
  • Lung Diseases / etiology
  • Lung Diseases / pathology*
  • Lysosomes / physiology
  • Mice
  • Mice, Knockout
  • Organelles
  • Stress, Physiological
  • TOR Serine-Threonine Kinases / antagonists & inhibitors

Substances

  • MTOR protein, human
  • TOR Serine-Threonine Kinases