Autophagy in pulmonary diseases. Review uri icon

Overview

MeSH

  • Animals
  • Apoptosis
  • Blood Vessels
  • Cystic Fibrosis
  • Emphysema
  • Humans
  • Hypertension, Pulmonary
  • Hypoxia
  • Immunity, Innate
  • Inflammation
  • Pulmonary Circulation
  • Pulmonary Disease, Chronic Obstructive
  • Smoking

MeSH Major

  • Autophagy
  • Lung Diseases

abstract

  • (Macro)autophagy provides a membrane-dependent mechanism for the sequestration, transport, and lysosomal turnover of subcellular components, including proteins and organelles. In this capacity, autophagy maintains basal cellular homeostasis and healthy organelle populations such as mitochondria. During starvation, autophagy prolongs cell survival by recycling metabolic precursors from intracellular macromolecules. Furthermore, autophagy represents an inducible response to chemical and physical cellular stress. Increasing evidence suggests that autophagy, and its regulatory proteins, may critically influence vital cellular processes such as programmed cell death, cell proliferation, inflammation, and innate immune functions and thereby may play a critical role in the pathogenesis of human disease. The function of autophagy in disease pathogenesis remains unclear and may involve either impaired or accelerated autophagic activity or imbalances in the activation of autophagic proteins. This review examines the roles of autophagy in the pathogenesis of pulmonary diseases, with emphasis on pulmonary vascular disease and acute and chronic lung diseases.

publication date

  • 2012

has subject area

  • Animals
  • Apoptosis
  • Autophagy
  • Blood Vessels
  • Cystic Fibrosis
  • Emphysema
  • Humans
  • Hypertension, Pulmonary
  • Hypoxia
  • Immunity, Innate
  • Inflammation
  • Lung Diseases
  • Pulmonary Circulation
  • Pulmonary Disease, Chronic Obstructive
  • Smoking

Research

keywords

  • Journal Article
  • Review

Identity

Language

  • eng

Digital Object Identifier (DOI)

  • 10.1146/annurev-physiol-020911-153348

PubMed ID

  • 22035347

Additional Document Info

start page

  • 377

end page

  • 401

volume

  • 74