O'Rourke B
Institute of Molecular Cardiobiology, Division of Cardiology, Department of Medicine, Johns Hopkins University, Baltimore, MD, USA.
Circ Res. 2000 Nov 10;87(10):845-55. doi: 10.1161/01.res.87.10.845.
We are on the brink of harnessing the cell's natural defenses against ischemia and reperfusion injury after years of research into the destructive and protective mechanisms involved. Since the discovery of ischemic preconditioning, the surface receptors and signal transduction pathways underlying this phenomenon have been clarified, but many questions remain about the downstream targets that ultimately protect the cell. ATP-sensitive K(+) (K(ATP)) channels are thought to play a role in protection, but their mechanism of action has been unclear. Accumulating evidence now suggests that the location of the K(ATP) channels relevant to cytoprotection may be on the mitochondrial inner membrane instead of on the sarcolemma of the cardiac cell. This review discusses recent findings and unanswered questions about the role of K(ATP) channels in preconditioning and protection.
经过多年对缺血和再灌注损伤相关的破坏及保护机制的研究,我们即将能够利用细胞自身的防御机制。自缺血预处理被发现以来,这一现象背后的表面受体和信号转导通路已得到阐明,但关于最终保护细胞的下游靶点仍有许多问题。ATP敏感性钾(K(ATP))通道被认为在保护过程中发挥作用,但其作用机制尚不清楚。现在越来越多的证据表明,与细胞保护相关的K(ATP)通道的位置可能在线粒体内膜而非心肌细胞的肌膜上。这篇综述讨论了关于K(ATP)通道在预处理和保护中的作用的最新发现及未解决的问题。