帮助 关于我们

返回检索结果

核苷酸结合寡聚化结构域样受体3炎症小体与阿尔茨海默病
Nucleotide-binding Oligomerization Domain-like Receptor Family Pyrin Domain Containing 3 Inflammasome in Alzheimer’s Disease

查看参考文献55篇

冯芸颖 1   陈慧 2 *  
文摘 阿尔茨海默病(AD)是一种慢性神经退行性疾病,发病原因至今未明。聚集在大脑内部的β淀粉样蛋白斑块是AD的主要病理特征之一,然而靶向细胞外β淀粉样蛋白斑块的药物均未能治愈疾病。固有免疫应答与神经炎症在AD的发病及进展中发挥重要作用。小胶质细胞作为中枢神经系统中的巨噬细胞,参与细胞外β淀粉样蛋白沉积、细胞内tau蛋白形成神经原纤维缠结和神经元损伤过程。越来越多的研究显示,小胶质细胞中核苷酸结合寡聚化结构域样受体3 (NLRP3)炎症小体的激活与AD的发生和发展相关,提示该信号通路可能是治疗AD的新靶点。本文总结了NLRP3炎症小体激活与调节在AD中的作用机制及以该通路为靶标治疗AD的研究现状,以期为未来该领域的研究提供参考。
其他语种文摘 Alzheimer’s disease (AD) is a chronic neurodegenerative disease whose cause remains unclear. The β-amyloid plaques in the brain are one of the major pathological features of AD. However,the drugs targeting extracellular β-amyloid plaques have failed to cure the disease. Innate immunity and neuroinflammation play a role in the pathogenesis and progression of AD. As the macrophages existing in the central nervous system, microglia are related with extracellular β-amyloid deposition,intracellular neurofibrillary tangle formation,and neuron injury. Accumulating evidence demonstrates that the activation of nucleotide-binding oligomerization domain- like receptor family pyrin domain containing 3 (NLRP3) inflammasome in microglia plays a role in AD, suggesting new therapeutic target for AD in this signaling pathway. This article reviewed the studies about the activation and regulation of NLRP3 inflammasome in the pathogenesis and progression of AD as well as the development of AD therapies targeting this pathway,aiming to provide reference for further studies in this field.
来源 中国医学科学院学报 ,2021,43(5):788-795 【核心库】
DOI 10.3881/j.issn.1000-503X.12585
关键词 核苷酸结合寡聚化结构域样受体3炎症小体 ; β淀粉样蛋白 ; 小胶质细胞 ; 阿尔茨海默病
地址

1. 中国医学科学院北京协和医学院基础学院, 北京, 100730  

2. 中国医学科学院北京协和医学院基础医学研究所免疫学系, 北京, 100005

语种 中文
文献类型 研究性论文
ISSN 1000-503X
学科 神经病学与精神病学
基金 国家自然科学基金 ;  国家自然基金委联合基金
文献收藏号 CSCD:7089731

参考文献 共 55 共3页

1.  Alzheimer's Disease International. World Alzheimer report 2019: attitudes to dementia,2019:10-12 CSCD被引 1 次    
2.  Nichols E. Global,regional, and national burden of Alzheimer's disease and other dementias, 1990-2016: a systematic analysis for the Global Burden of Disease Study 2016. Lancet Neurol,2019,18(1):88-106 CSCD被引 12 次    
3.  Mathys H. Single-cell transcriptomic analysis of Alzheimer's disease. Nature,2019,570(7761):332-337 CSCD被引 53 次    
4.  Constantinescu C S. Astrocytes as antigen-presenting cells: expression of IL-12/IL-23. J Neurochem,2005,95(2):331-340 CSCD被引 6 次    
5.  Halle A. The NALP3 inflammasome is involved in the innate immune response to amyloid-β. Nat Immunol,2008,9(8):857-865 CSCD被引 116 次    
6.  Martinon F. The inflammasome: a molecular platform triggering activation of inflammatory caspases and processing of proIL-β. Mol Cell,2002,10(2):417-426 CSCD被引 257 次    
7.  Man S M. Converging roles of caspases in inflammasome activation,cell death and innate immunity. Nat Rev Immunol,2016,16(1):7-21 CSCD被引 49 次    
8.  Man S M. Regulation of inflammasome activation. Immunol Rev,2015,265(1):6-21 CSCD被引 61 次    
9.  Bauernfeind F G. Cutting edge: NF-κB activating pattern recognition and cytokine receptors license NLRP3 inflammasome activation by regulating NLRP3 expression. J Immunol,2009,183(2):787-791 CSCD被引 160 次    
10.  Xue Y. Emerging activators and regulators of inflammasomes and pyroptosis. Trends Immunol,2019,40(11):1035-1052 CSCD被引 43 次    
11.  Shi J. Cleavage of GSDMD by inflammatory caspases determines pyroptotic cell death. Nature,2015,526(7575):660-665 CSCD被引 427 次    
12.  Shi H. NLRP3 activation and mitosis are mutually exclusive events coordinated by NEK7,a new inflammasome component. Nat Immunol,2016,17(3):250-258 CSCD被引 34 次    
13.  Schmid-Burgk J L. A genomewide CRISPR (clustered regularly interspaced short palindromic repeats) screen identifies NEK7 as an essential component of NLRP3 inflammasome activation. J Biol Chem,2016,291(1):103-109 CSCD被引 23 次    
14.  Sharif H. Structural mechanism for NEK7-licensed activation of NLRP3 inflammasome. Nature,2019,570(7761):338-343 CSCD被引 57 次    
15.  Munoz-Planillo R. K~+ efflux is the common trigger of NLRP3 inflammasome activation by bacterial toxins and particulate matter. Immunity,2013,38(6):1142-1153 CSCD被引 90 次    
16.  Petrilli V. Activation of the NALP3 inflammasome is triggered by low intracellular potassium concentration. Cell Death Differ,2007,14(9):1583-1589 CSCD被引 58 次    
17.  Lee G S. The calcium-sensing receptor regulates the NLRP3 inflammasome through Ca~(2 +) and cAMP. Nature,2012,492(7427):123-127 CSCD被引 51 次    
18.  Katsnelson M A. K~+ efflux agonists induce NLRP3 inflammasome activation independently of Ca~(2 +) signaling. J Immunol,2015,194(8):3937-3952 CSCD被引 18 次    
19.  Tang T. CLICs-dependent chloride efflux is an essential and proximal upstream event for NLRP3 inflammasome activation. Nat Commun,2017,8(1):1-12 CSCD被引 27 次    
20.  Meissner F. Superoxide dismutase 1 regulates caspase-1 and endotoxic shock. Nat Immunol,2008,9(8):866-872 CSCD被引 6 次    
引证文献 1 篇

1 王虎平 从"肝肾同调"探析黑逍遥散干预AD免疫炎症的研究思路 中国实验方剂学杂志,2022,28(17):180-187
CSCD被引 4 次

显示所有1篇文献

论文科学数据集
PlumX Metrics
相关文献

 作者相关
 关键词相关
 参考文献相关

版权所有 ©2008 中国科学院文献情报中心 制作维护：中国科学院文献情报中心
地址：北京中关村北四环西路33号 邮政编码：100190 联系电话：(010)82627496 E-mail:cscd@mail.las.ac.cn 京ICP备05002861号-4 | 京公网安备11010802043238号