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本文引用的文献

1
Pyroptotic neuronal cell death mediated by the AIM2 inflammasome.AIM2 炎性小体介导的细胞焦亡性神经元死亡。
J Cereb Blood Flow Metab. 2014 Apr;34(4):621-9. doi: 10.1038/jcbfm.2013.236. Epub 2014 Jan 8.
2
Salmonella infection induces recruitment of Caspase-8 to the inflammasome to modulate IL-1β production.沙门氏菌感染诱导 Caspase-8 募集到炎症小体以调节 IL-1β 的产生。
J Immunol. 2013 Nov 15;191(10):5239-46. doi: 10.4049/jimmunol.1301581. Epub 2013 Oct 11.
3
Caspase-11: the driving factor for noncanonical inflammasomes.Caspase-11:非典型炎性小体的驱动因素。
Eur J Immunol. 2013 Sep;43(9):2240-5. doi: 10.1002/eji.201343800.
4
Activation and regulation of the inflammasomes.炎症小体的激活与调控。
Nat Rev Immunol. 2013 Jun;13(6):397-411. doi: 10.1038/nri3452.
5
Inflammasome and cytokine blocking strategies in autoinflammatory disorders.自身炎症性疾病中炎性小体和细胞因子阻断策略。
Clin Immunol. 2013 Jun;147(3):242-75. doi: 10.1016/j.clim.2013.04.008. Epub 2013 Apr 19.
6
The NLRP3 inflammasome in Alzheimer's disease.NLRP3 炎性小体在阿尔茨海默病中的作用。
Mol Neurobiol. 2013 Dec;48(3):875-82. doi: 10.1007/s12035-013-8475-x. Epub 2013 May 19.
7
Inhibition of phagocytosis and lysosomal acidification suppresses neurotoxic prion peptide-induced NALP3 inflammasome activation in BV2 microglia.抑制吞噬作用和溶酶体酸化可抑制神经毒性朊病毒肽诱导的 BV2 小胶质细胞 NALP3 炎性体激活。
J Neuroimmunol. 2013 Jul 15;260(1-2):121-5. doi: 10.1016/j.jneuroim.2013.04.016. Epub 2013 May 13.
8
Promises and pitfalls of a Pannexin1 transgenic mouse line.Pannexin1 转基因小鼠品系的优缺点。
Front Pharmacol. 2013 May 9;4:61. doi: 10.3389/fphar.2013.00061. eCollection 2013.
9
Human astrocytes express a novel NLRP2 inflammasome.人类星形胶质细胞表达一种新型 NLRP2 炎性小体。
Glia. 2013 Jul;61(7):1113-21. doi: 10.1002/glia.22499. Epub 2013 Apr 26.
10
Alarmins, inflammasomes and immunity.警报素、炎性小体与免疫。
Biomed J. 2012 Nov-Dec;35(6):437-49. doi: 10.4103/2319-4170.104408.

细胞焦亡体的激活与调控:中枢神经系统损伤相关研究中的知识缺口。

Activation and regulation of cellular inflammasomes: gaps in our knowledge for central nervous system injury.

机构信息

Department of Neurological Surgery, The Miami Project to Cure Paralysis, Lois Pope LIFE Center, Miami, Florida, USA.

Department of Physiology and Biophysics, University of Miami Miller School of Medicine, Miami, Florida, USA.

出版信息

J Cereb Blood Flow Metab. 2014 Mar;34(3):369-75. doi: 10.1038/jcbfm.2013.227. Epub 2014 Jan 8.

DOI:10.1038/jcbfm.2013.227
PMID:24398940
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3948131/
Abstract

The inflammasome is an intracellular multiprotein complex involved in the activation of caspase-1 and the processing of the proinflammatory cytokines interleukin-1β (IL-1β) and IL-18. The inflammasome in the central nervous system (CNS) is involved in the generation of an innate immune inflammatory response through IL-1 cytokine release and in cell death through the process of pyroptosis. In this review, we consider the different types of inflammasomes (NLRP1, NLRP2, NLRP3, and AIM2) that have been described in CNS cells, namely neurons, astrocytes, and microglia. Importantly, we focus on the role of the inflammasome after brain and spinal cord injury and cover the potential activators of the inflammasome after CNS injury such as adenosine triphosphate and DNA, and the therapeutic potential of targeting the inflammasome to improve outcomes after CNS trauma.

摘要

炎症小体是一种细胞内多蛋白复合物,参与半胱氨酸蛋白酶-1 的激活和前炎症细胞因子白细胞介素-1β(IL-1β)和 IL-18 的加工。中枢神经系统(CNS)中的炎症小体通过白细胞介素 1 细胞因子释放参与固有免疫炎症反应的产生,并通过细胞焦亡过程导致细胞死亡。在这篇综述中,我们考虑了已在 CNS 细胞(即神经元、星形胶质细胞和小胶质细胞)中描述的不同类型的炎症小体(NLRP1、NLRP2、NLRP3 和 AIM2)。重要的是,我们专注于炎症小体在脑和脊髓损伤后的作用,并涵盖了 CNS 损伤后炎症小体的潜在激活剂,如三磷酸腺苷和 DNA,以及靶向炎症小体以改善 CNS 创伤后结局的治疗潜力。