Hypoxia and ischemia-reperfusion: a BiK contribution?
Hypoxia and ischemia-reperfusion: a BiK contribution?
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缺氧和缺血再灌注：BiK 的贡献？
DOI：
10.1152/ajpheart.00319.2014
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发表时间：
2014
期刊：
影响因子：
--
通讯作者：
Gollasch M
中科院分区：
文献类型：
--
作者：
Tano JY;Gollasch M
在过去的几十年里，心血管疾病已经成为西方世界死亡的主要原因，而且这一趋势正在全世界蔓延。特别是，动脉粥样硬化和随后的血管闭塞是缺血性疾病（中风和冠心病）的主要原因。过量钙流入细胞是人类脑和心脏缺血损伤的重要病理生理机制之一。因此，大电导钙激活的K+通道（BK）是防止过量钙流入和导致缺血性损伤事件的有趣候选者。事实上，线粒体BK通道（mitoBK）最近在体外和动物模型中都被证明对缺血再灌注损伤具有保护作用，尽管这种保护的确切机制仍在研究中。此外，在质膜和线粒体BK通道中，α-亚基本身对缺氧都很敏感。这种敏感性是组织特异性的，并由通道胞内C端富含半胱氨酸的选择性剪接插入（STREX）内高度保守的基序赋予。这篇综述描述了BK通道在缺氧和缺血再灌注损伤中日益增加的相关性的最新进展。
Over the last decades, cardiovascular disease has become the primary cause of death in the Western world, and this trend is expanding throughout the world. In particular, atherosclerosis and the subsequent vessel obliterations are the primary cause of ischemic disease (stroke and coronary heart disease). Excess calcium influx into the cells is one of the major pathophysiological mechanisms important for ischemic injury in the brain and heart in humans. The large-conductance calcium-activated K+channels (BK) are thus interesting candidates to protect against excess calcium influx and the events leading to ischemic injury. Indeed, the mitochondrial BK channels (mitoBK) have recently been shown to play a protective function against ischemia-reperfusion injury both in vitro and in animal models, although the exact mechanism of this protection is still under scrutiny. In addition, in both the plasma membrane and mitochondrial BK channel, the α-subunit itself is sensitive to hypoxia. This sensitivity is tissue specific and conferred by a highly conserved motif within an alternatively spliced cysteine-rich insert (STREX) in the intracellular C terminus of the channel. This review describes recent developments of the increasing relevance of BK channels in hypoxia and ischemia-reperfusion injury.
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