Negative regulation of NLRP3 inflammasome signaling.
10.1007/s13238-013-2128-8
- Author:
Shuzhen CHEN
1
;
Bing SUN
Author Information
1. State Key Laboratory of Cell Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes of Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China.
- Publication Type:Journal Article
- MeSH:
Animals;
Autophagy;
Carrier Proteins;
antagonists & inhibitors;
metabolism;
Caspase 1;
metabolism;
Humans;
Inflammasomes;
metabolism;
Interferon Type I;
metabolism;
MicroRNAs;
metabolism;
NLR Family, Pyrin Domain-Containing 3 Protein;
Nitric Oxide;
metabolism;
Signal Transduction;
T-Lymphocytes;
immunology;
metabolism
- From:
Protein & Cell
2013;4(4):251-258
- CountryChina
- Language:English
-
Abstract:
Inflammasomes are multiprotein complexes that serve as a platform for caspase-1 activation and interleukin-1β (IL-1β) maturation as well as pyroptosis. Though a number of inflammasomes have been described, the NLRP3 inflammasome is the most extensively studied. NLRP3 inflammasome is triggered by a variety of stimuli, including infection, tissue damage and metabolic dysregulation, and then activated through an integrated cellular signal. Many regulatory mechanisms have been identified to attenuate NLRP3 inflammasome signaling at multiple steps. Here, we review the developments in the negative regulation of NLRP3 inflammasome that protect host from inflammatory damage.
