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线粒体 K(ATP) 通道——事实还是虚构?

The mitochondrial K(ATP) channel--fact or fiction?

机构信息

Department of Biology, Portland State University, Portland, OR 97201-0751, USA.

出版信息

J Mol Cell Cardiol. 2012 Mar;52(3):578-83. doi: 10.1016/j.yjmcc.2011.12.011. Epub 2012 Jan 2.

DOI:10.1016/j.yjmcc.2011.12.011
PMID:22240339
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3617982/
Abstract

The mitochondrial ATP-dependent K(+) channel (mitoK(ATP)) is widely considered by many to play a central role in cardioprotection by ischemic and pharmacological preconditioning and by ischemic postconditioning. Nevertheless, several laboratories have questioned the existence of mitoK(ATP). This article summarizes the evidence for and against and addresses two key questions: How strong is the evidence for the presence of a K(ATP) channel in mitochondria? Are the pharmacological agents used to modulate mitoK(ATP) activity sufficiently specific to allow the role of these channels in cardioprotection to be established?

摘要

线粒体三磷酸腺苷依赖性钾(mitoKATP)通道被许多人广泛认为在缺血和药物预处理以及缺血后处理的心脏保护中发挥核心作用。然而,一些实验室对 mitoKATP 的存在提出了质疑。本文总结了支持和反对的证据,并回答了两个关键问题:证明线粒体中存在 KATP 通道的证据有多强?用于调节 mitoKATP 活性的药物在多大程度上足够特异,以确定这些通道在心脏保护中的作用?

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Mitochondrial approaches to protect against cardiac ischemia and reperfusion injury.用于预防心脏缺血再灌注损伤的线粒体方法。
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The mitochondrial complex II and ATP-sensitive potassium channel interaction: quantitation of the channel in heart mitochondria.线粒体复合物II与ATP敏感性钾通道的相互作用:心脏线粒体中该通道的定量分析
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Mechanism of cardioprotection by early ischemic preconditioning.早期缺血预处理的心脏保护机制。
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Cardioprotective mechanisms of mitochondria-targeted S-nitrosating agent and adenosine triphosphate-sensitive potassium channel opener are mutually exclusive.线粒体靶向性S-亚硝基化剂与三磷酸腺苷敏感性钾通道开放剂的心脏保护机制相互排斥。
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