Mitochondria: Sovereign of inflammation?

Détails

ID Serval
serval:BIB_0F29C2536C44
Type
Article: article d'un périodique ou d'un magazine.
Sous-type
Synthèse (review): revue aussi complète que possible des connaissances sur un sujet, rédigée à partir de l'analyse exhaustive des travaux publiés.
Collection
Publications
Institution
Titre
Mitochondria: Sovereign of inflammation?
Périodique
European Journal of Immunology
Auteur(s)
Tschopp J.
ISSN
1521-4141 (Electronic)
ISSN-L
0014-2980
Statut éditorial
Publié
Date de publication
2011
Volume
41
Numéro
5
Pages
1196-1202
Langue
anglais
Résumé
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 ROS, which is required for inflammasome activation. On the contrary, 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.
Mots-clé
Animals, Autophagy, Carrier Proteins/metabolism, Humans, Immunity, Innate, Inflammasomes/immunology, Inflammasomes/metabolism, Inflammation/immunology, Inflammation/metabolism, Interleukin-1beta/immunology, Interleukin-1beta/metabolism, Mice, Mitochondria/metabolism, Mitochondria/pathology, Reactive Oxygen Species/metabolism, Signal Transduction
Pubmed
Web of science
Open Access
Oui
Création de la notice
02/09/2011 9:59
Dernière modification de la notice
20/08/2019 13:35
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