内质网应激调控NLRP3炎症小体的研究进展

被引:23
作者
陈淑珍
机构
[1] 厦门医学院病原生物与免疫学教研室
关键词
内质网应激; NLRP3炎症小体; 未折叠蛋白反应; 炎症性疾病;
D O I
暂无
中图分类号
R363 [病理生理学];
学科分类号
100103 [病原生物学];
摘要
内质网是真核细胞中负责蛋白合成和折叠的重要细胞器,当未折叠或错误折叠蛋白在内质网腔内累积引起内质网应激时,内质网通过启动未折叠蛋白反应维持细胞稳态。炎症小体是细胞内的一种多蛋白复合物,活化后剪切Pro-Caspase-1,产生IL-1β等促炎因子,引发细胞焦亡,在固有免疫和适应性免疫中均发挥重要作用。在目前已知的多种炎症小体中,NLRP3炎症小体研究得最为深入。近年来研究表明,内质网应激与NLRP3炎症小体有密切联系,参与调控NLRP3炎症小体的活化,并在炎症性疾病的发生发展中起重要作用。本文对内质网应激参与调控NLRP3炎症小体的相关研究进展进行简要综述。
引用
收藏
页码:905 / 910
页数:6
相关论文
共 17 条
[1]
降钙素基因相关肽通过降低炎性小体活性抑制巨噬细胞功能 [J].
刘元 ;
郭俊峰 ;
蔡俊 ;
杨阳 ;
李鑫 ;
张慧宇 ;
张纲 .
免疫学杂志, 2017, (05) :400-404
[2]
High fat diet dysregulates microRNA-17-5p and triggers retinal inflammation: Role of endoplasmic-reticulum-stress[J] Maha Coucha;Islam N Mohamed;Sally L Elshaer;Osinakachuk Mbata;Megan L Bartasis;Azza B El-Remessy; World Journal of Diabetes 2017,
[3]
Mechanism and Regulation of NLRP3 Inflammasome Activation[J] Yuan He;Hideki Hara;Gabriel Núñez Trends in Biochemical Sciences 2016,
[4]
Role of Mitochondria-Associated Endoplasmic Reticulum Membrane in Inflammation-Mediated Metabolic Diseases[J] Themis Thoudam;Jae-Han Jeon;Chae-Myeong Ha;In-Kyu Lee;Helen C. Steel Mediators of Inflammation 2016,
[5]
Endoplasmic Reticulum Chaperon Tauroursodeoxycholic Acid Attenuates Aldosterone-Infused Renal Injury[J] Honglei Guo;Hongmei Li;Lilu Ling;Yong Gu;Wei Ding;Christian Bowman-Colin Mediators of Inflammation 2016,
[6]
Pharmacological activation of AMPK prevents Drp1-mediated mitochondrial fission and alleviates endoplasmic reticulum stress-associated endothelial dysfunction[J] Jia Li;Yilei Wang;Yapu Wang;Xiaodong Wen;Xiao-Nan Ma;Weijie Chen;Fang Huang;Junping Kou;Lian-Wen Qi;Baolin Liu;Kang Liu Journal of Molecular and Cellular Cardiology 2015,
[7]
Ilexgenin A inhibits endoplasmic reticulum stress and ameliorates endothelial dysfunction via suppression of TXNIP/NLRP3 inflammasome activation in an AMPK dependent manner[J] Yi Li;Jie Yang;Mei-Hong Chen;Qiang Wang;Min-Jian Qin;Tong Zhang;Xiao-Qing Chen;Bao-Lin Liu;Xiao-Dong Wen Pharmacological Research 2015,
[8]
Astragaloside IV and cycloastragenol are equally effective in inhibition of endoplasmic reticulum stress-associated TXNIP/NLRP3 inflammasome activation in the endothelium[J] Yan Zhao;Qiang Li;Wenjun Zhao;Jia Li;Yan Sun;Kang Liu;Baolin Liu;Ning Zhang Journal of Ethnopharmacology 2015,
[9]
Endoplasmic Reticulum Stress Activates the Inflammasome via NLRP3- and Caspase-2-Driven Mitochondrial Damage[J] Denise N. Bronner;Basel H. Abuaita;Xiaoyun Chen;Katherine A. Fitzgerald;Gabriel Nuñez;Yongqun He;Xiao-Ming Yin;Mary X.D. O’Riordan Immunity 2015,
[10]
Initiation and perpetuation of NLRP 3 inflammasome activation and assembly[J] Eric I. Elliott;Fayyaz S. Sutterwala Immunol Rev 2015,