The Relationship between Mitochondria and NLRP3 Inflammasome.
10.11620/IJOB.2017.42.3.085
- Author:
Hyun Ah LEE
1
;
Hee Sam NA
;
Jin CHUNG
Author Information
1. Department of Oral Microbiology, School of Dentistry, Pusan National University, Yangsan 50162, Korea. jchung@pusan.ac.kr
- Publication Type:Review
- Keywords:
Mitochondria;
NLRP3 inflammasome;
Innate immune response
- MeSH:
Adenosine Triphosphate;
Calcium;
Cardiolipins;
DNA, Mitochondrial;
Homeostasis;
Immunity, Innate;
Inflammasomes*;
Inflammation;
Metabolic Networks and Pathways;
Mitochondria*;
Mitochondrial Degradation;
NAD;
Reactive Oxygen Species
- From:International Journal of Oral Biology
2017;42(3):85-90
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Mitochondria participate in various intracellular metabolic pathways such as generating intracellular ATP, synthesizing several essential molecules, regulating calcium homeostasis, and producing the cell's reactive oxygen species (ROS). Emerging studies have demonstrated newly discovered roles of mitochondria, which participate in the regulation of innate immune responses by modulating NLRP3 inflammasomes. Here, we review the recently proposed pathways to be involved in mitochondria-mediated regulation of inflammasome activation and inflammation: 1) mitochondrial ROS, 2) calcium mobilization, 3) nicotinamide adenine dinucleotide (NAD+) reduction, 4) cardiolipin, 5) mitofusin, 6) mitochondrial DNA, 7) mitochondrial antiviral signaling protein. Furthermore, we highlight the significance of mitophagy as a negative regulator of mitochondrial damage and NLRP3 inflammasome activation, as potentially helpful therapeutic approaches which could potentially address uncontrolled inflammation.
