The role of mitochondria in NLRP3 inflammasome activation

被引：347

作者：

Liu, Qiuyun ^{[1
]}

Zhang, Danyan ^{[1
]}

Hu, Diyu ^{[1
]}

Zhou, Xiangmei ^{[2
]}

Zhou, Yang ^{[1
]}

机构：

[1] Southwest Univ, Coll Anim Sci, Chongqing 402460, Peoples R China

[2] China Agr Univ, Natl Anim Transmissible Spongiform Encephalopathy, State Key Labs Agrobiotechnol, Key Lab Anim Epidemiol,Minist Agr,Coll Vet Med, Beijing 100193, Peoples R China

来源：

MOLECULAR IMMUNOLOGY | 2018年 / 103卷

关键词：

Reactive oxygen species; mtDNA; Cardiolipin; Ubiquitination; Calcium; NF-KAPPA-B; ENDOPLASMIC-RETICULUM; PERMEABILITY TRANSITION; NALP3; INFLAMMASOME; INTERLEUKIN-1-BETA RELEASE; HOST-DEFENSE; MITOFUSIN; CELL-DEATH; PROTEIN; APOPTOSIS;

D O I：

10.1016/j.molimm.2018.09.010

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

070307 [化学生物学]; 071010 [生物化学与分子生物学];

摘要：

The NLRP3 inflammasome is a multiprotein platform which is activated upon cellular infection or stress. Its activation leads to caspase-1-dependent secretion of proinflammatory cytokines like interleukin-1 beta (IL-1 beta) and IL-18, and an inflammatory form of cell death termed as pyroptosis. Recent studies have unveiled the pivotal roles of mitochondria in initiation and regulation of the NLRP3 (nucleotide-binding domain, leucine-rich-repeat containing family, pyrin domain-containing 3) inflammasome. NLRP3 activators induce mitochondrial destabilization, NLRP3 deubiquitination, linear ubiquitination of ASC, and externalization or release of mitochondria derived molecules such as cardiolipin and mitochondrial DNA. These molecules bind to NLRP3 that is translocated on mitochondria and activate the NLRP3 inflammasome. Here we review recently described mechanisms by which mitochondria regulate NLRP3 inflammasome activation.

引用

收藏

页码：115 / 124

页数：10

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