The role of Nod-like receptor protein 3 inflammasome activated by ion channels in multiple diseases.
The role of Nod-like receptor protein 3 inflammasome activated by ion channels in multiple diseases.
复制标题
离子通道激活的nod样受体蛋白3炎性小体在多种疾病中的作用
DOI：
10.1007/s11010-022-04602-1
复制
发表时间：
2023-06
影响因子：
4.3
通讯作者：
Xie R
中科院分区：
文献类型：
--
作者：
Xu X;Wu X;Yue G;An Q;Lou J;Yang X;Jin Z;Ding J;Hu Y;Du Q;Xu J;Xie R
炎性小体是位于细胞质中的多聚体蛋白复合物，被多种因子激活，随后促进促炎因子如白细胞介素（IL）-1β和IL-18的释放，导致一系列炎症反应，最终导致各种疾病的发生。Nod样受体蛋白3（Nod-like receptor protein 3，NLRP 3）炎性小体是目前研究最多、最具特征的炎性小体。NLRP 3炎性体的激活与许多疾病的发生密切相关，如阿尔茨海默病。目前，大量的研究集中在NLRP 3炎性体激活的潜在机制。大量文献报道了多种离子如K+、Na+回流和Ca 2+内流对NLRP 3炎性小体的激活作用。然而，很少有文章综述了各种离子通道对NLRP 3炎性体激活的影响以及这些蛋白引起的疾病之间的关系。本文主要综述了细胞内外离子活性和离子通道与NLRP 3炎性体激活的关系。我们还提供了由NLRP 3激活引起的每个系统的疾病的一般总结。我们希望更多的研究将为治疗由NLRP 3炎性小体驱动的疾病提供选择。
The inflammasome is a multimeric protein complex located in the cytoplasm that is activated by many factors and subsequently promotes the release of proinflammatory factors such as interleukin (IL)-1β and IL-18, resulting in a series of inflammatory responses that ultimately lead to the occurrence of various diseases. The Nod-like receptor protein 3 (NLRP3) inflammasome is the most characteristic type and the most widely studied among many inflammasomes. Activation of the NLRP3 inflammasome is closely related to the occurrence of many diseases, such as Alzheimer's disease. At present, a large number of studies have focused on the mechanisms underlying the activation of the NLRP3 inflammasome. Plenty of articles have reported the activation of the NLRP3 inflammasome by various ions, such as K+ and Na+ reflux and Ca2+ influx. However, few articles have reviewed the effects of various ion channels on the activation of the NLRP3 inflammasome and the relationship between the diseases caused by these proteins. This article mainly summarizes the relationship between intracellular and extracellular ion activities and ion channels and the activation of the NLRP3 inflammasome. We also provide a general summary of the diseases of each system caused by NLRP3 activation. We hope that more research will provide options for the treatment of diseases driven by the NLRP3 inflammasome.
登录
查看更多内容
影响因子：
16.6
作者：
Daniels MJ;Rivers-Auty J;Schilling T;Spencer NG;Watremez W;Fasolino V;Booth SJ;White CS;Baldwin AG;Freeman S;Wong R;Latta C;Yu S;Jackson J;Fischer N;Koziel V;Pillot T;Bagnall J;Allan SM;Paszek P;Galea J;Harte MK;Eder C;Lawrence CB;Brough D
通讯作者：
Brough D
星形胶质细胞上的 Kir6.1/K-ATP 通道通过促进线粒体自噬预防帕金森病 MPTP 小鼠模型中的多巴胺能神经变性
影响因子：
15.1
作者：
Hu, Zhao-Li;Sun, Ting;Hu, Gang
通讯作者：
Hu, Gang
DOI：
10.1016/j.bbalip.2019.04.001
发表时间：
2019-07-01
影响因子：
4.8
作者：
Gianfrancesco, Marco A.;Dehairs, Jonas;Legrand-Poels, Sylvie
通讯作者：
Legrand-Poels, Sylvie
Kir6.2敲除通过增强NLRP3炎症小体激活加重脂多糖诱导的小鼠肝损伤
影响因子：
6.3
作者：
Du, Ren-Hong;Tan, Jun;Hu, Gang
通讯作者：
Hu, Gang
影响因子：
6.2
作者：
通讯作者：
--