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本文引用的文献

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Coupling of phosphorylation to electron and hydrogen transfer by a chemi-osmotic type of mechanism.通过化学渗透机制将磷酸化与电子及氢转移相偶联。
Nature. 1961 Jul 8;191:144-8. doi: 10.1038/191144a0.
2
Molecular composition of mitochondrial ATP-sensitive potassium channels probed by viral Kir gene transfer.通过病毒Kir基因转移探究线粒体ATP敏感性钾通道的分子组成
J Mol Cell Cardiol. 2000 Nov;32(11):1923-30. doi: 10.1006/jmcc.2000.1226.
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The machinery of local Ca2+ signalling between sarco-endoplasmic reticulum and mitochondria.肌浆网与线粒体之间局部钙离子信号传导机制。
J Physiol. 2000 Nov 15;529 Pt 1(Pt 1):69-81. doi: 10.1111/j.1469-7793.2000.00069.x.
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Mitochondrial intermembrane junctional complexes and their role in cell death.线粒体膜间隙连接复合体及其在细胞死亡中的作用。
J Physiol. 2000 Nov 15;529 Pt 1(Pt 1):11-21. doi: 10.1111/j.1469-7793.2000.00011.x.
5
Mitochondrial uncoupling proteins: from mitochondria to the regulation of energy balance.线粒体解偶联蛋白:从线粒体到能量平衡的调节
J Physiol. 2000 Nov 15;529 Pt 1(Pt 1):3-10. doi: 10.1111/j.1469-7793.2000.00003.x.
6
Selective pharmacological agents implicate mitochondrial but not sarcolemmal K(ATP) channels in ischemic cardioprotection.选择性药理制剂表明,线粒体而非肌膜的ATP敏感性钾通道参与缺血性心脏保护作用。
Circulation. 2000 May 23;101(20):2418-23. doi: 10.1161/01.cir.101.20.2418.
7
Outer mitochondrial membrane permeability can regulate coupled respiration and cell survival.线粒体外膜通透性可调节偶联呼吸和细胞存活。
Proc Natl Acad Sci U S A. 2000 Apr 25;97(9):4666-71. doi: 10.1073/pnas.090082297.
8
ATP-Sensitive potassium channels: a review of their cardioprotective pharmacology.ATP敏感性钾通道:其心脏保护药理学综述
J Mol Cell Cardiol. 2000 Apr;32(4):677-95. doi: 10.1006/jmcc.2000.1111.
9
Preservation of mitochondrial function by diazoxide during sustained ischaemia in the rat heart.二氮嗪在大鼠心脏持续性缺血期间对线粒体功能的保护作用。
Br J Pharmacol. 2000 Mar;129(6):1219-27. doi: 10.1038/sj.bjp.0703148.
10
Preconditioning in cardiomyocytes protects by attenuating oxidant stress at reperfusion.心肌细胞中的预处理通过减轻再灌注时的氧化应激来发挥保护作用。
Circ Res. 2000 Mar 17;86(5):541-8. doi: 10.1161/01.res.86.5.541.

线粒体离子通道的病理生理及保护作用

Pathophysiological and protective roles of mitochondrial ion channels.

作者信息

O'Rourke B

机构信息

Institute of Molecular Cardiobiology, Division of Cardiology, Department of Medicine, The Johns Hopkins University, Baltimore, MD 21205, USA.

出版信息

J Physiol. 2000 Nov 15;529 Pt 1(Pt 1):23-36. doi: 10.1111/j.1469-7793.2000.00023.x.

DOI:10.1111/j.1469-7793.2000.00023.x
PMID:11080248
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2270186/
Abstract

Mitochondria possess a highly permeable outer membrane and an inner membrane that was originally thought to be relatively impermeable to ions to prevent dissipation of the electrochemical gradient for protons. Although recent evidence has revealed a rich diversity of ion channels in both membranes, the purpose of these channels remains incompletely determined. Pores in the outer membrane are fundamental participants in apoptotic cell death, and this process may also involve permeability transition pores on the inner membrane. Novel functions are now being assigned to other ion channels of the inner membrane. Examples include protection against ischaemic injury by mitochondrial KATP channels and the contribution of inner membrane anion channels to spontaneous mitochondrial oscillations in cardiac myocytes. The central role of mitochondria in both the normal function of the cell and in its demise makes these channels prime targets for future research and drug development.

摘要

线粒体具有高度可渗透的外膜和内膜,内膜最初被认为对离子相对不可渗透,以防止质子电化学梯度的消散。尽管最近的证据表明这两种膜中存在丰富多样的离子通道,但这些通道的功能仍未完全确定。外膜中的孔是凋亡细胞死亡的基本参与者,这个过程也可能涉及内膜上的通透性转换孔。现在,内膜的其他离子通道也被赋予了新的功能。例如,线粒体ATP敏感性钾通道对缺血性损伤具有保护作用,内膜阴离子通道对心肌细胞中线粒体的自发振荡有贡献。线粒体在细胞正常功能及其死亡过程中都起着核心作用,这使得这些通道成为未来研究和药物开发的主要靶点。