Autophagy in Inflammatory Diseases

Autophagy provides a mechanism for the turnover of cellular organelles and proteins through a lysosome-dependent degradation pathway. During starvation, autophagy exerts a homeostatic function that promotes cell survival by recycling metabolic precursors. Additionally, autophagy can interact with ot...

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Main Authors: Alexander J. S. Choi, Stefan W. Ryter
Format: Article
Language:English
Published: Wiley 2011-01-01
Series:International Journal of Cell Biology
Online Access:http://dx.doi.org/10.1155/2011/732798
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author Alexander J. S. Choi
Stefan W. Ryter
author_facet Alexander J. S. Choi
Stefan W. Ryter
author_sort Alexander J. S. Choi
collection DOAJ
description Autophagy provides a mechanism for the turnover of cellular organelles and proteins through a lysosome-dependent degradation pathway. During starvation, autophagy exerts a homeostatic function that promotes cell survival by recycling metabolic precursors. Additionally, autophagy can interact with other vital processes such as programmed cell death, inflammation, and adaptive immune mechanisms, and thereby potentially influence disease pathogenesis. Macrophages deficient in autophagic proteins display enhanced caspase-1-dependent proinflammatory cytokine production and the activation of the inflammasome. Autophagy provides a functional role in infectious diseases and sepsis by promoting intracellular bacterial clearance. Mutations in autophagy-related genes, leading to loss of autophagic function, have been implicated in the pathogenesis of Crohn's disease. Furthermore, autophagy-dependent mechanisms have been proposed in the pathogenesis of several pulmonary diseases that involve inflammation, including cystic fibrosis and pulmonary hypertension. Strategies aimed at modulating autophagy may lead to therapeutic interventions for diseases associated with inflammation.
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spelling doaj-art-072d4bd8fe29443f92916a31f01eab652025-02-03T05:54:00ZengWileyInternational Journal of Cell Biology1687-88761687-88842011-01-01201110.1155/2011/732798732798Autophagy in Inflammatory DiseasesAlexander J. S. Choi0Stefan W. Ryter1College of Arts and Sciences, Boston College, 140 Commonwealth Avenue, Chestnut Hill, MA 02467, USAPulmonary and Critical Care Medicine, Brigham and Women's Hospital, Harvard Medical School, 75 Francis Street, Boston, MA 02115, USAAutophagy provides a mechanism for the turnover of cellular organelles and proteins through a lysosome-dependent degradation pathway. During starvation, autophagy exerts a homeostatic function that promotes cell survival by recycling metabolic precursors. Additionally, autophagy can interact with other vital processes such as programmed cell death, inflammation, and adaptive immune mechanisms, and thereby potentially influence disease pathogenesis. Macrophages deficient in autophagic proteins display enhanced caspase-1-dependent proinflammatory cytokine production and the activation of the inflammasome. Autophagy provides a functional role in infectious diseases and sepsis by promoting intracellular bacterial clearance. Mutations in autophagy-related genes, leading to loss of autophagic function, have been implicated in the pathogenesis of Crohn's disease. Furthermore, autophagy-dependent mechanisms have been proposed in the pathogenesis of several pulmonary diseases that involve inflammation, including cystic fibrosis and pulmonary hypertension. Strategies aimed at modulating autophagy may lead to therapeutic interventions for diseases associated with inflammation.http://dx.doi.org/10.1155/2011/732798
spellingShingle Alexander J. S. Choi
Stefan W. Ryter
Autophagy in Inflammatory Diseases
International Journal of Cell Biology
title Autophagy in Inflammatory Diseases
title_full Autophagy in Inflammatory Diseases
title_fullStr Autophagy in Inflammatory Diseases
title_full_unstemmed Autophagy in Inflammatory Diseases
title_short Autophagy in Inflammatory Diseases
title_sort autophagy in inflammatory diseases
url http://dx.doi.org/10.1155/2011/732798
work_keys_str_mv AT alexanderjschoi autophagyininflammatorydiseases
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