| Mitochondria: sovereign of inflammation? | |
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MedLine Citation:
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PMID: 21469137 Owner: NLM Status: Publisher |
Abstract/OtherAbstract:
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NLRP3-inflammasome dependent inflammatory responses are triggered by a variety of signals of host danger, including infection, tissue damage and metabolic dysregulation. How these diverse activators cause inflammasome activation is poorly understood. Recent data suggest that the mitochondria integrate these distinct signals and relay this information to the NLRP3 inflammasome. Dysfunctional mitochondria generate reactive oxygen species (ROS), which is required for inflammasome activation. In contrast, the NLRP3 inflammasome is negatively regulated by autophagy, which is a catabolic process that removes damaged or otherwise dysfunctional organelles, including mitochondria. In addition to the processing and secretion of pro-inflammatory cytokines such as IL-1β NLRP3 inflammasome activation also influences cellular metabolic pathways such as glycolysis and lipogenesis. Mapping the connections between mitochondria, metabolism and inflammation is of great interest, as malfunctioning of this network is associated with many chronic inflammatory diseases. |
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Authors:
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Jürg Tschopp |
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Publication Detail:
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Type: JOURNAL ARTICLE Date: 2011-3-18 |
Journal Detail:
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Title: European journal of immunology Volume: - ISSN: 1521-4141 ISO Abbreviation: - Publication Date: 2011 Mar |
Date Detail:
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Created Date: 2011-4-6 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 1273201 Medline TA: Eur J Immunol Country: - |
Other Details:
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Languages: ENG Pagination: - Citation Subset: - |
Copyright Information:
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Copyright © 2011 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim. |
Affiliation:
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Department of Biochemistry, University of Lausanne, Center for Immunity and Infection, Chemin des Boveresses 155, CH-1066 Epalinges, Switzerland. jurg.tschopp@unil.ch. |
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