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.

Key words: cerebral ischemia, gap junction, connexin 43 hemichannel, inflammation, NLRP3