Mitochondria: Joining forces to thwart cell death

Mitochondria: Joining forces to thwart cell death
复制标题

DOI:
10.1016/j.bbadis.2009.09.006
复制
发表时间:
2010-01-01
影响因子:
6.2
通讯作者:
Slack, Ruth S.
Slack, Ruth S.
中科院分区:
生物学2区
文献类型:
--
作者:
Jahani-Asl, Arezu;Germain, Marc;Slack, Ruth S.

文献摘要

被引文献

相似文献

线粒体是高度动态的细胞器,经历融合和分裂的恒定循环。线粒体功能的另一个调节水平是它们沿沿着的主动运输,这在神经元中特别重要。最近的证据表明,线粒体融合/裂变机制以及负责其运动的分子马达构成了直接影响代谢和细胞死亡调节的强大调节控制点。这不仅适用于细胞凋亡,也适用于兴奋性毒性,其中钙超载是细胞死亡过程的主要组成部分。在这篇综述中,我们将描述调节融合和分裂的分子机制,以及在急性神经元损伤的背景下,这如何影响细胞存活。(C)2009 Elsevier B. V.保留所有权利。
Mitochondria are highly dynamic organelles that undergo constant cycles of fusion and fission. An additional level of regulation of mitochondrial function, which is particularly important in neurons, is their active transport along microtubules. Recent evidence suggests that the mitochondrial fusion/fission machinery as well as the molecular motors responsible for their movement constitute powerful regulatory control points that directly impact metabolism and regulation of cell death. This is true for not only apoptosis, but also for excitotoxicity where calcium overload is a major component of the cell death process. In this review, we will describe the molecular mechanisms regulating fusion and fission and how this impinges on cell survival in the context of acute neuronal injury. (C) 2009 Elsevier B.V. All rights reserved.