Mitochondrial fragmentation in neurodegeneration

被引:788
作者
Knott, Andrew B. [1 ]
Perkins, Guy [2 ]
Schwarzenbacher, Robert [3 ]
Bossy-Wetzel, Ella [1 ]
机构
[1] Univ Cent Florida, Coll Med, Burnett Sch Biomed Sci, Orlando, FL 32816 USA
[2] Univ Calif San Diego, Sch Med, Natl Ctr Microscopy & Imaging Res, La Jolla, CA 92093 USA
[3] Salzburg Univ, Dept Mol Biol, A-5020 Salzburg, Austria
关键词
D O I
10.1038/nrn2417
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Mitochondria are remarkably dynamic organelles that migrate, divide and fuse. Cycles of mitochondrial fission and fusion ensure metabolite and mitochondrial DNA mixing and dictate organelle shape, number and bioenergetic functionality. There is mounting evidence that mitochondrial dysfunction is an early and causal event in neurodegeneration. Mutations in the mitochondrial fusion GTPases mitofusin 2 and optic atrophy 1, neurotoxins and oxidative stress all disrupt the cable-like morphology of functional mitochondria. This results in impaired bioenergetics and mitochondrial migration, and can trigger neurodegeneration. These findings suggest potential new treatment avenues for neurodegenerative diseases.
引用
收藏
页码:505 / 518
页数:14
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