Related Experiment Video
Updated: Mar 5, 2026

Two-vessel Occlusion Mouse Model of Cerebral Ischemia-reperfusion
Published on: March 1, 2019
Connexins and Pannexins in cerebral ischemia
Yeri Kim1, Joanne O Davidson2, Colin R Green1
1Department of Ophthalmology, Faculty of Medical and Health Sciences, University of Auckland.
Insights
Cerebral ischemia, a brain blood flow loss, causes cell death via inflammatory pathways. Connexin and Pannexin channels are key targets for treating this condition.
Area of Science:
- Neuroscience
- Cell Biology
- Pathology
Background:
- Cerebral ischemia, or brain ischemia, is a leading cause of death and adult disability globally.
- It results from sudden blood flow loss, leading to unmet brain metabolic demands and cell death.
- Inflammatory pathways are activated, causing irreversible brain tissue damage.
Purpose of the Study:
- To review the roles of Connexin and Pannexin channels in cerebral ischemia-induced cell death.
- To highlight these channels as potential therapeutic targets for brain ischemia.
- To focus on connexin hemichannels' role in ATP release during ischemia and reperfusion.
Main Methods:
- Literature review of studies on Connexins and Pannexins in cerebral ischemia.
- Analysis of the time-dependent roles of these channels in ischemic injury.
- Examination of their involvement in cell death mechanisms and ATP release.
Main Results:
- Connexin and Pannexin channels play significant, time-dependent roles in perpetuating ischemic injury.
- Connexin hemichannels are implicated in substantial ATP release during both ischemia and reperfusion.
- These channels are involved in various cell death pathways following ischemic events.
Conclusions:
- Connexin and Pannexin channels represent promising therapeutic targets for mitigating cerebral ischemia.
- Targeting connexin hemichannels may offer a strategy to reduce ischemia-reperfusion injury.
- Further research into these channels could lead to novel treatments for brain ischemia and its consequences.
Abstract:
A common cause of mortality and long-term adult disability, cerebral ischemia or brain ischemia imposes a significant health and financial burden on communities worldwide. Cerebral ischemia is a condition that arises from a sudden loss of blood flow and consequent failure to meet the high metabolic demands of the brain. The lack of blood flow initiates a sequelae of cell death mechanisms, including the activation of the inflammatory pathway, which can ultimately result in irreversible brain tissue damage. In particular, Connexins and Pannexins are non-selective channels with a large pore that have shown to play time-dependent roles in the perpetuation of ischaemic injury. This review highlights the roles of Connexin and Pannexin channels in cell death mechanisms as a promising therapeutic target in cerebral ischemia, and in particular connexin hemichannels which may contribute most of the ATP release as a result of ischemia as well as during reperfusion. This article is part of a Special Issue entitled: Gap Junction Proteins edited by Jean Claude Herve.
Related Concept Videos
Gap Junctions
Gap Junctions

