Inflammasomes and Cell Death: Common Pathways in Microparticle Diseases.
Animals
Cell Communication
/ drug effects
Cell Death
Cell-Derived Microparticles
/ metabolism
Cellular Microenvironment
Disease Susceptibility
/ etiology
Humans
Inflammasomes
/ metabolism
Interleukin-1beta
/ metabolism
NLR Family, Pyrin Domain-Containing 3 Protein
/ metabolism
Pyroptosis
Signal Transduction
/ drug effects
NLRP3
atherosclerosis
inflammasome
necroptosis
neuroinflammation
pyroptosis
Journal
Trends in molecular medicine
ISSN: 1471-499X
Titre abrégé: Trends Mol Med
Pays: England
ID NLM: 100966035
Informations de publication
Date de publication:
11 2020
11 2020
Historique:
received:
18
02
2020
revised:
02
06
2020
accepted:
04
06
2020
pubmed:
11
7
2020
medline:
16
10
2021
entrez:
11
7
2020
Statut:
ppublish
Résumé
The accumulation of cellular and environmental microparticles has been linked to many diseases associated with tissue inflammation. These particulate-driven diseases include joint, lung, kidney, cardiovascular, and neurodegenerative disorders. Recently a conserved proinflammatory inflammasome signaling pathway elicited by such microparticles has become apparent. Here, we review disease-promoting microparticles and the mechanisms by which they trigger activation of the inflammasome complexes responsible for generating bioactive interleukin-1β (IL-1β) and inducing cell death. We highlight how microparticle-induced inflammasome and cell death responses diverge from canonical inflammasome activators, and discuss the preclinical and clinical targeting of inflammasomes to treat microparticle-driven diseases.
Identifiants
pubmed: 32646646
pii: S1471-4914(20)30156-8
doi: 10.1016/j.molmed.2020.06.005
pii:
doi:
Substances chimiques
IL1B protein, human
0
Inflammasomes
0
Interleukin-1beta
0
NLR Family, Pyrin Domain-Containing 3 Protein
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
1003-1020Informations de copyright
Crown Copyright © 2020. Published by Elsevier Ltd. All rights reserved.