线粒体
生物
细胞生物学
神经科学
细胞内
细胞器
轴浆运输
生物学中的钙
程序性细胞死亡
平衡
运动前神经元活动
钙信号传导
细胞凋亡
生物化学
作者
Diane T. W. Chang,Ian J. Reynolds
标识
DOI:10.1016/j.pneurobio.2006.09.003
摘要
Mitochondria are the primary generators of ATP and are important regulators of intracellular calcium homeostasis. These organelles are dynamically transported along lengthy neuronal processes, presumably for appropriate distribution to cellular regions of high metabolic demand and elevated intracellular calcium, such as synapses. The removal of damaged mitochondria that produce harmful reactive oxygen species and promote apoptosis is also thought to be mediated by transport of mitochondria to autophagosomes. Mitochondrial trafficking is therefore important for maintaining neuronal and mitochondrial health while cessation of movement may lead to neuronal and mitochondrial dysfunction. Mitochondrial morphology is also dynamic and is remodeled during neuronal injury and disease. Recent studies reveal different manifestations and mechanisms of impaired mitochondrial movement and altered morphology in injured neurons. These are likely to cause varied courses toward neuronal degeneration and death. The goal of this review is to provide an appreciation of the full range of mitochondrial function, morphology and trafficking, and the critical role these parameters play in neuronal physiology and pathophysiology.
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