Mitostasis in Neurons: Maintaining Mitochondria in an Extended Cellular Architecture.,Neuron

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Mitostasis in Neurons: Maintaining Mitochondria in an Extended Cellular Architecture.
Neuron ( IF 14.7 ) Pub Date : 2017-Nov-01 , DOI: 10.1016/j.neuron.2017.09.055
Thomas Misgeld ₁ , Thomas L Schwarz ₂

Affiliation

Neurons have more extended and complex shapes than other cells and consequently face a greater challenge in distributing and maintaining mitochondria throughout their arbors. Neurons can last a lifetime, but proteins turn over rapidly. Mitochondria, therefore, need constant rejuvenation no matter how far they are from the soma. Axonal transport of mitochondria and mitochondrial fission and fusion contribute to this rejuvenation, but local protein synthesis is also likely. Maintenance of a healthy mitochondrial population also requires the clearance of damaged proteins and organelles. This involves degradation of individual proteins, sequestration in mitochondria-derived vesicles, organelle degradation by mitophagy and macroautophagy, and in some cases transfer to glial cells. Both long-range transport and local processing are thus at work in achieving neuronal mitostasis-the maintenance of an appropriately distributed pool of healthy mitochondria for the duration of a neuron's life. Accordingly, defects in the processes that support mitostasis are significant contributors to neurodegenerative disorders.

中文翻译：

神经元的有丝分裂：在扩展的细胞结构中维持线粒体。

神经元比其他细胞具有更广泛和更复杂的形状，因此在整个乔木中分布和维持线粒体方面面临更大的挑战。神经元可以持续一生，但蛋白质周转速度很快。因此，无论离体细胞多远，线粒体都需要不断恢复活力。线粒体的轴突运输和线粒体裂变和融合有助于这种复兴，但也可能是局部蛋白质合成。维持健康的线粒体种群还需要清除受损的蛋白质和细胞器。这涉及单个蛋白质的降解、线粒体衍生的囊泡中的隔离、线粒体自噬和巨自噬引起的细胞器降解，以及在某些情况下转移到神经胶质细胞。因此，远程运输和局部处理都在实现神经元有丝分裂——在神经元的生命周期内维持适当分布的健康线粒体池。因此，支持有丝分裂的过程中的缺陷是导致神经退行性疾病的重要因素。

更新日期：2017-11-01

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