Connexin 43 hemichannel mediates NLRP3 inflammasome activation and its role in cerebral ischemia
10.3969/j.issn.1006-5725.2024.10.021
- VernacularTitle:连接蛋白43半通道介导NLRP3炎症小体激活在脑缺血中的作用
- Author:
Linhui PENG
1
;
Dan LI
;
Zhiqiang HU
;
Xialin ZUO
Author Information
1. 广州医科大学神经科学研究所,广州医科大学附属第二医院神经内科(广州 510260)
- Keywords:
cerebral ischemia;
gap junction;
connexin 43 hemichannel;
inflammation;
NLRP3
- From:
The Journal of Practical Medicine
2024;40(10):1450-1454
- CountryChina
- Language:Chinese
-
Abstract:
Gap junction proteins have a significant impact on the propagation of neuroinflammation after cerebral ischemia.Connexin 43(Cx43),the principal connexin in the central nervous system,typically assembles hexameric hemichannels in an oligomeric state that dock with hemichannels on adjacent cells to form gap junction channels.Ordinarily,the likelihood of cell surface hemichannels opening is minimal.However,during cerebral ischemia,the excessive activation of Cx43 hemichannels leads to the liberation of a substantial quantity of ions(Na+,Cl-,Ca2+,and K+),glutamate,aspartate,and adenosine triphosphate(ATP),thereby resulting in impairment of adjacent cells and aggravation of neuronal injury.Furthermore,the activation of Cx43 hemichannels triggers the release of inflammatory factors,which exhibits a strong association with the activation of NLRP3 inflammasome after cerebral ischemia.Hence,the modulation of Cx43 hemichannels presents a potential avenue for mitigating neuroinflammation and subsequently diminishing cerebral ischemic injury.This article focuses on the relationship between Cx43 hemichannels and NLRP3 inflammasome activation,as well as its role in cerebral ischemia,all of which provide novel insights and therapeutic approaches for managing cerebral ischemia.
