线粒体通道及其在心脏保护中的作用

Keerti Mishra, Min Luo
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引用次数: 2

摘要

线粒体在心脏保护中起着关键作用。主要的心脏保护机制是缺血预处理(IpreC),通过这种机制,短时间的缺血可以保护随后延长的急性缺血发作。线粒体通道,特别是钾通道(mitoK),如atp依赖性和钙激活的钾通道,被认为是IpreC的触发物或末端效应器。mitoK激活剂是一种很有前途的治疗缺血性心肌损伤的药物。在本章中,我们总结了我们目前对不同线粒体通道的生理功能的了解,重点是钾通道及其在心脏保护中的机制。此外,还讨论了目前正在开发的靶向线粒体通道治疗心力衰竭的治疗方法。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Mitochondrial Channels and their Role in Cardioprotection
Mitochondria play a pivotal role in cardioprotection. The major cardioprotective mechanism is ischemic preconditioning (IpreC), through which short periods of ischemia protect a subsequent prolonged acute ischemic episode. Mitochondria channels, particularly the potassium channels (mitoK) such as ATP-dependent and calcium-activated potassium channels, have been suggested as trigger or end effectors in IpreC. Activators of mitoK are promising therapeutic agents for the treatment of the myocardial injury due to ischemic episodes. In this chapter, we are summarizing our current knowledge on the physiology function of different mitochondrial channels with a focus on the potassium channels and their mechanism in cardioprotection. Furthermore, the currently under development therapy by targeting the mitochondrial channels for the treatment of heart failure are also discussed.
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