Surveillance and transportation of mitochondria in neurons
Surveillance and transportation of mitochondria in neurons
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DOI：
10.1016/j.conb.2019.01.015
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发表时间：
2019-08-01
影响因子：
5.7
通讯作者：
Wang, Xinnan
中科院分区：
文献类型：
--
作者：
Vanhauwaert, Roeland;Bharat, Vinita;Wang, Xinnan
神经元需要分配和维持线粒体，以提供足够的能量和足够的Ca2+缓冲能力，在其广泛的分支的每个亚专业化。受损的线粒体对神经元非常有害，必须迅速修复或清除，即使它们被留在离体细胞极远的末端。神经元独特的形状使线粒体的运输和清除任务变得复杂。潜在分子调控的错误导致有害的神经退行性变。在这里，我们回顾了用于在神经元中运输、分布和清除线粒体的分子机制和调节机制，以及这些基本调节如何在神经系统疾病中受到损害。
Neurons need to allocate and sustain mitochondria to provide adequate energy and sufficient Ca2+-buffering capacity in each sub specialization of their extensive arborizations. Damaged mitochondria, which are highly deleterious to the neuron, must be rapidly repaired or eliminated, even when they are left at terminals extremely far away from the soma. The unique shape of neurons complicates the tasks of both transporting and clearing mitochondria. Errors in the underlying molecular regulations cause detrimental neurodegeneration. Here, we review the molecular machinery and regulatory mechanisms employed to transport, distribute, and clear mitochondria in neurons, and how these fundamental regulations are compromised in neurological disorders.