Inflammation initiated by stressed organelles.

Détails

Ressource 1Télécharger: Martinon.pdf (1605.30 [Ko])
Etat: Public
Version: Author's accepted manuscript
Licence: Non spécifiée
ID Serval
serval:BIB_18E9EB64E09E
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
Inflammation initiated by stressed organelles.
Périodique
Joint, bone, spine
Auteur(s)
Martinon F.
ISSN
1778-7254 (Electronic)
ISSN-L
1297-319X
Statut éditorial
Publié
Date de publication
07/2018
Peer-reviewed
Oui
Volume
85
Numéro
4
Pages
423-428
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't ; Review
Publication Status: ppublish
Résumé
Key cellular functions including those related to energy metabolism, organization of the genetic information or production of membrane-bound and secreted proteins are compartmentalized within organelles. Various stresses such as differentiation programs, viral and bacterial infections, perturbations in protein production, mechanical constraints, changes in the environment and nutriment accessibility can impact cellular homeostasis and organelle integrity. Perturbations of these cellular compartments trigger repair and adaptation programs aimed at restoring homeostasis. These events are often associated with low-grade inflammation also termed parainflammation. While the nature and mechanisms of danger signals released by irremediably damaged cells are well understood, how transiently stressed cells trigger inflammation is still poorly understood. Emerging studies highlighted new mechanisms by which stress pathways promote inflammation. Cytosolic innate immune pathways are engaged by signals stemming from perturbed organelles such as the mitochondria, the endoplasmic reticulum (ER) or the nuclear envelope (NE). These observations indicate that these pathways function as guardians of cellular homeostasis and may contribute to disease in pathologies characterized by perturbations of cellular homoeostasis. Mitochondria-stress, ER-stress or NE-stress are emerging as proinflammatory signals that contribute to human conditions and diseases.
Mots-clé
Animals, Arthritis, Rheumatoid/immunology, Arthritis, Rheumatoid/metabolism, Cell Differentiation/immunology, Endoplasmic Reticulum/immunology, Endoplasmic Reticulum/metabolism, Endoplasmic Reticulum Stress/immunology, Homeostasis/immunology, Humans, Inflammasomes/immunology, Inflammasomes/metabolism, Inflammation/immunology, Inflammation/metabolism, Mitochondria/immunology, Mitochondria/metabolism, Sensitivity and Specificity, Signal Transduction/immunology, ER-stress, Inflammasome, Mitochondria, Nuclear envelope
Pubmed
Web of science
Financement(s)
Fonds national suisse / Projets / 310030173152
Création de la notice
21/11/2017 13:15
Dernière modification de la notice
29/04/2020 6:20
Données d'usage