Percolation and criticality in a mitochondrial network
Percolation and criticality in a mitochondrial network
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DOI：
10.1073/pnas.0307156101
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发表时间：
2004-03-30
影响因子：
11.1
通讯作者：
O'Rourke, B
中科院分区：
文献类型：
--
作者：
Aon, MA;Cortassa, S;O'Rourke, B
线粒体功能的同步化是细胞生理和存活的重要决定因素，但对细胞器间通讯的机制知之甚少。我们最近观察到，心脏细胞线粒体能量状态的协调细胞范围内的振荡可以通过线粒体网络的一些元素的高度局部化扰动来诱导，这表明线粒体代表了一个复杂的自组织系统。在这里，我们应用渗滤理论来解释线粒体信号传播的机制，在响应氧化应激。一个全球性的相变（线粒体去极化）显示发生时，线粒体的临界密度积累活性氧超过阈值，形成一个扩展的跨越集群。线粒体网络在不稳定边缘的标度和分形特性与线粒体被组织为渗透矩阵的想法非常一致，活性氧是关键的信使。
Synchronization of mitochondrial function is an important determinant of cell physiology and survival, yet little is known about the mechanism of interorganellar communication. We have recently observed that coordinated cell-wide oscillations in the mitochondrial energy state of heart cells can be induced by a highly localized perturbation of a few elements of the mitochondrial network, indicating that mitochondria represent a complex, self-organized system. Here, we apply percolation theory to explain the mechanism of intermitochondrial signal propagation in response to oxidative stress. A global phase transition (mitochondrial depolarization) is shown to occur when a critical density of mitochondria accumulate reactive oxygen species above a threshold to form an extended spanning cluster. The scaling and fractal properties of the mitochondrial network at the edge of instability agree remarkably well with the idea that mitochondria are organized as a percolation matrix, with reactive oxygen species as a key messenger.