Lipid regulation of NLRP3 inflammasome activity through organelle stress

被引：33
作者：
Liang, Jonathan J. [1 ,2 ]
Fraser, Lain D. C. [1 ]
Bryant, Clare E. [2 ]
机构：
[1] NIAID, Signaling Syst Sect, Lab Immune Syst Biol, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA
[2] Univ Cambridge, Dept Med, Cambridge, England
来源：
TRENDS IN IMMUNOLOGY | 2021年 / 42卷 / 09期
关键词：
LOW-DENSITY-LIPOPROTEIN; ENDOPLASMIC-RETICULUM STRESS; SATURATED FATTY-ACIDS; FOAM CELL-FORMATION; INSULIN-RESISTANCE; OXIDIZED LDL; GASDERMIN D; NONALCOHOLIC STEATOHEPATITIS; MITOCHONDRIAL DYSFUNCTION; CARDIOVASCULAR-DISEASE;
D O I：
10.1016/j.it.2021.07.005
中图分类号：
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号：
100102 ;
摘要：
Inflammation driven by the NLRP3 inflammasome in macrophages is an important contributor to chronic metabolic diseases that affect growing numbers of indi-viduals. Many of these diseases involve the pathologic accumulation of en-dogenous lipids or their oxidation products, which can activate NLRP3. Other endogenous lipids, however, can inhibit the activation of NLRP3. The intracellular mechanisms by which these lipids modulate NLRP3 activity are now being identi-fied. This review discusses emerging evidence suggesting that organelle stress, particularly involving mitochondria, lysosomes, and the endoplasmic reticulum, may be key in lipid-induced modification of NLRP3 inflammasome activity.
引用
收藏
页码：807 / 823
页数：17
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