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首页> 外文期刊>Biochimica et biophysica acta. Biomembranes >Connexins and Pannexins in cerebral ischemia
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Connexins and Pannexins in cerebral ischemia

机译：Connexins和脑缺血中的Pannexins

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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. Highlights ? Glutamatergic transmission may have time-dependent effects on connexin- and pannexin-channel activity post ischemic injury. ? Connexin hemichannels may contribute most of the ATP release as a result of ischemia. ? Pannexin channels and Connexin hemichannels are the key players in the release of nucleotides into the extracellular space, which initiates an inflammatory response. ? Connexin hemichannels play a role in increasing BBB permeability in response to inflammation by spreading Calcium waves, releasing ATP, and causing vascular endothelial cell death. ? Sheep, rat, and mouse models have been used to study the role of hemichannels and the effect of channel blockade in cerebral ischemia. ? Both pannexin channel and connexin hemichannel block has been shown to be beneficial during and after cerebral ischaemic injury and such treatments offer significant therapeutic potential.
机译：摘要死亡率和长期成人残疾，脑缺血或脑缺血的常见原因对全球社区产生了重大的健康和财务负担。脑缺血是一种突然丧失血流丧失的条件，从而达到大脑的高代谢需求。缺乏血液流动引发了一种细胞死亡机制的后遗症，包括激活炎症途径，最终可能导致不可逆的脑组织损伤。特别地，Connexins和Pannexins是具有大孔的非选择性通道，其显示在缺血性损伤的永久性中发挥时间依赖的作用。本综述突出了Connexin和Pannexin通道在细胞死亡机制中作为脑缺血的有希望的治疗靶标的作用，特别是Connexin血管笼，其可能导致缺血以及再灌注期间的缺血以及在再灌注过程中产生的大部分ATP释放。本文是题为的特殊问题的一部分：Jean Claude Herve编辑的Gap Junction蛋白。强调 ？谷氨酸酯透射率可能对Connexin和Pannexin-Channel活性的时间依赖性作用缺血性损伤。还Connexin Hemickannels可能导致缺血导致的大部分ATP释放。还Pannexin通道和Connexin Hemichannels是核苷酸进入细胞外空间的关键球员，其引起炎症反应。还Connexin Hemichannels在通过扩散钙波，释放ATP并导致血管内皮细胞死亡，在增加炎症时发挥作用。还绵羊，大鼠和小鼠模型已被用于研究血管箱的作用以及通道阻滞在脑缺血中的作用。还在脑缺血性损伤期间和后，Pannexin通道和Connexin Hemichannel障碍块都被证明是有益的，并且这种治疗具有显着的治疗潜力。

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