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Miro MCU and calcium: bridging our understanding of mitochondrial movement in axons

机译:MiroMCU和钙:桥接我们对轴突线粒体运动的理解

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摘要

Neurons are extremely polarized structures with long axons and dendrites, which require proper distribution of mitochondria and maintenance of mitochondrial dynamics for neuronal functions and survival. Indeed, recent studies show that various neurological disorders are linked to mitochondrial transport in neurons. Mitochondrial anterograde transport is believed to deliver metabolic energy to synaptic terminals where energy demands are high, while mitochondrial retrograde transport is required to repair or remove damaged mitochondria in axons. It has been suggested that Ca2+ plays a key role in regulating mitochondrial transport by altering the configuration of mitochondrial protein, miro. However, molecular mechanisms that regulate mitochondrial transport in neurons still are not well characterized. In this review, we will discuss the roles of miro in mitochondrial transport and how the recently identified components of the mitochondrial calcium uniporter add to our current model of mitochondrial mobility regulation.
机译:神经元是具有长轴突和树突的极端极化的结构,需要线粒体的适当分布和线粒体动力学的维持才能使神经元功能和生存。实际上,最近的研究表明,各种神经系统疾病与神经元中的线粒体运输有关。线粒体顺行运输被认为是向能量需求高的突触末端传递代谢能量,而线粒体逆行运输则需要修复或去除轴突中受损的线粒体。有人认为,Ca 2 + 通过改变线粒体蛋白miro的构型在调节线粒体运输中起关键作用。但是,调节神经元中线粒体运输的分子机制仍未很好地表征。在这篇综述中,我们将讨论miro在线粒体运输中的作用,以及最近发现的线粒体钙单向转运体的成分如何添加到我们当前的线粒体活动性调节模型中。

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