Autophagy: Friend or Foe in Lung Disease? Review uri icon

Overview

MeSH

  • Disease Progression
  • Humans

MeSH Major

  • Apoptosis
  • Autophagy
  • Homeostasis
  • Lung
  • Lung Diseases

abstract

  • Autophagy is a highly conserved process by which cells can recycle organelles and proteins by degrading them in the lysosomes. Although autophagy is considered a dynamic system responsible for cellular renovation and homeostasis under physiological conditions, it is increasingly clear that autophagy is directly relevant to clinical disease. During disease progression, autophagy not only serves as a cellular protective mechanism but also can represent a harmful event under certain conditions. In addition, although autophagy can act as a nonselective bulk degradation process, recent research shows that autophagy can selectively degrade specific proteins, organelles, and invading bacteria, in processes termed "selective autophagy." Selective autophagy has drawn the attention of researchers because of its potential importance in clinical diseases. In this article, we outline the most recent studies implicating autophagy and selective autophagy in human lung diseases, including chronic obstructive pulmonary disease, pulmonary hypertension, idiopathic pulmonary fibrosis, and sepsis. We also discuss the relationship between autophagy and other molecular mechanisms related to disease progression, including programmed necrosis (necroptosis) and the inflammasome, an inflammatory signaling platform that regulates the secretion of IL-1β and IL-18. Finally, we examine the dual nature of autophagy and selective autophagy in the lung, which have both protective and injurious effects for human lung disease.

publication date

  • March 2016

has subject area

  • Apoptosis
  • Autophagy
  • Disease Progression
  • Homeostasis
  • Humans
  • Lung
  • Lung Diseases

Research

keywords

  • Journal Article
  • Review

Identity

Language

  • eng

Digital Object Identifier (DOI)

  • 10.1513/AnnalsATS.201507-450MG

PubMed ID

  • 27027951

Additional Document Info

start page

  • S40

end page

  • S47

volume

  • 13 Suppl 1