Autophagy in pulmonary diseases

Stefan W. Ryter, Kiichi Nakahira, Jeffrey A. Haspel, Augustine M.K. Choi

Research output: Contribution to journalArticle

73 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)377-401
Number of pages25
JournalAnnual review of physiology
Volume74
DOIs
StatePublished - 2012

Keywords

  • Apoptosis
  • Autophagosome
  • Cell proliferation
  • Chronic obstructive pulmonary disease
  • Cigarette smoke
  • Hypoxia
  • Inflammation
  • Pulmonary hypertension

ASJC Scopus subject areas

  • Physiology

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