线粒体融合
线粒体分裂
MFN1型
线粒体
神经退行性变
生物
细胞生物学
细胞器
神经科学
裂变
线粒体DNA
遗传学
医学
物理
疾病
病理
基因
中子
量子力学
作者
Ambre M. Bertholet,Thomas Delerue,Aurélie Millet,Manon Moulis,Claudine David,Marlène Daloyau,Laetitia Pelloquin,Noélie Davezac,Valérie Mils,Marie‐Christine Miquel,Manuel Rojo,Pascale Belenguer
标识
DOI:10.1016/j.nbd.2015.10.011
摘要
Mitochondria are dynamic organelles that continually move, fuse and divide. The dynamic balance of fusion and fission of mitochondria determines their morphology and allows their immediate adaptation to energetic needs, keeps mitochondria in good health by restoring or removing damaged organelles or precipitates cells in apoptosis in cases of severe defects. Mitochondrial fusion and fission are essential in mammals and their disturbances are associated with several diseases. However, while mitochondrial fusion/fission dynamics, and the proteins that control these processes, are ubiquitous, associated diseases are primarily neurological disorders. Accordingly, inactivation of the main actors of mitochondrial fusion/fission dynamics is associated with defects in neuronal development, plasticity and functioning, both ex vivo and in vivo. Here, we present the central actors of mitochondrial fusion and fission and review the role of mitochondrial dynamics in neuronal physiology and pathophysiology. Particular emphasis is placed on the three main actors of these processes i.e. DRP1,MFN1-2, and OPA1 as well as on GDAP1, a protein of the mitochondrial outer membrane preferentially expressed in neurons. This article is part of a Special Issue entitled: Mitochondria & Brain.
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