title: Autophagy: a crucial moderator of redox balance, inflammation, and apoptosis in lung disease.
abstract: CONCLUSIONS
  Autophagy is a fundamental cellular process that functions in the turnover of subcellular organelles and protein. Activation of autophagy may represent a cellular defense against oxidative stress, or related conditions that cause accumulation of damaged proteins or organelles. Selective forms of autophagy can maintain organelle populations or remove aggregated proteins. Autophagy can increase survival during nutrient deficiency and play a multifunctional role in host defense, by promoting pathogen clearance and modulating innate and adaptive immune responses.
  
  
  BACKGROUND
  Autophagy has been described as an inducible response to oxidative stress. Once believed to represent a random process, recent studies have defined selective mechanisms for cargo assimilation into autophagosomes. Such mechanisms may provide for protein aggregate detoxification and mitochondrial homeostasis during oxidative stress. Although long studied as a cellular phenomenon, recent advances implicate autophagy as a component of human diseases. Altered autophagy phenotypes have been observed in various human diseases, including lung diseases such as chronic obstructive lung disease, cystic fibrosis, pulmonary hypertension, and idiopathic pulmonary fibrosis.
  
  
  RESULTS
  Although autophagy can represent a pro-survival process, in particular, during nutrient starvation, its role in disease pathogenesis may be multifunctional and complex. The relationship of autophagy to programmed cell death pathways is incompletely defined and varies with model system.
  
  
  CONCLUSIONS
  Activation or inhibition of autophagy may be used to alter the progression of human diseases. Further resolution of the mechanisms by which autophagy impacts the initiation and progression of diseases may lead to the development of therapeutics specifically targeting this pathway.
authors.affiliation: Division of Pulmonary and Critical Care Medicine, Department of Medicine, Brigham and Women's Hospital , Harvard Medical School, Boston, Massachusetts.
authors.forename: Kiichi
authors.initials: K
authors.lastname: Nakahira
authors.forename: Suzanne M
authors.initials: SM
authors.lastname: Cloonan
authors.forename: Kenji
authors.initials: K
authors.lastname: Mizumura
authors.forename: Augustine M K
authors.initials: AM
authors.lastname: Choi
authors.forename: Stefan W
authors.initials: SW
authors.lastname: Ryter
mesh_terms: D017209:Apoptosis / Q000235:genetics; D001343:Autophagy / Q000235:genetics* / Q000502:physiology; D006706:Homeostasis; D006801:Humans; D007249:Inflammation / Q000235:genetics / Q000378:metabolism / Q000503:physiopathology*; D008171:Lung Diseases / Q000235:genetics / Q000378:metabolism* / Q000503:physiopathology; D008928:Mitochondria / Q000378:metabolism / Q000473:pathology; D010084:Oxidation-Reduction; D018384:Oxidative Stress / Q000235:genetics / Q000502:physiology*; D010588:Phagosomes / Q000378:metabolism / Q000473:pathology