Biochem Soc Trans. 2013 Dec;41(6):1618-24. doi: 10.1042/BST20130189.
Mitochondrial dynamics are essential for maintaining organelle stability and function. Through fission, fusion and mitophagic events, optimal populations of mitochondria are retained. Subsequently, alterations in such processes can have profound effects on the individual mitochondrion and the cell within which they reside. Neurons are post-mitotic energy-dependent cells and, as such, are particularly vulnerable to alterations in cellular bioenergetics and increased stress that may occur as a direct or indirect result of mitochondrial dysfunction. The trafficking of mitochondria to areas of higher energy requirements, such as synapses, where mitochondrial densities fluctuate, further highlights the importance of efficient mitochondrial dynamics in neurons. PD (Parkinson's disease) is a common progressive neurodegenerative disorder which is characterized by the loss of dopaminergic neurons within the substantia nigra. Complex I, the largest of all of the components of the electron transport chain is heavily implicated in PD pathogenesis. The exact series of events that lead to cell loss, however, are not fully elucidated, but are likely to involve dysfunction of mitochondria, their trafficking and dynamics.
线粒体动力学对于维持细胞器的稳定性和功能至关重要。通过分裂、融合和噬线粒体事件，维持最佳的线粒体群体。随后，这些过程的改变可能对单个线粒体和细胞产生深远的影响。神经元是有丝分裂后依赖能量的细胞，因此，它们特别容易受到细胞生物能量的改变和增加的压力的影响，这些改变可能是线粒体功能障碍的直接或间接结果。线粒体向能量需求较高的区域（如突触）的运输，线粒体密度波动，进一步凸显了神经元中线粒体动力学的重要性。PD（帕金森病）是一种常见的进行性神经退行性疾病，其特征是黑质中多巴胺能神经元的丧失。复合体 I 是电子传递链中所有成分中最大的一个，与 PD 的发病机制密切相关。然而，导致细胞死亡的确切事件序列尚未完全阐明，但可能涉及线粒体功能障碍、它们的运输和动力学。
