线粒体生物学与帕金森病。
Mitochondrial biology and Parkinson's disease.
机构信息
Vall d'Hebron Research Institute-CIBERNED, Barcelona 08035, Spain.
出版信息
Cold Spring Harb Perspect Med. 2012 Feb;2(2):a009332. doi: 10.1101/cshperspect.a009332.
Abstract
Mitochondria are highly dynamic organelles with complex structural features which play several important cellular functions, such as the production of energy by oxidative phosphorylation, the regulation of calcium homeostasis, or the control of programmed cell death (PCD). Given its essential role in neuronal viability, alterations in mitochondrial biology can lead to neuron dysfunction and cell death. Defects in mitochondrial respiration have long been implicated in the etiology and pathogenesis of Parkinson's disease (PD). However, the role of mitochondria in PD extends well beyond defective respiration and also involves perturbations in mitochondrial dynamics, leading to alterations in mitochondrial morphology, intracellular trafficking, or quality control. Whether a primary or secondary event, mitochondrial dysfunction holds promise as a potential therapeutic target to halt the progression of dopaminergic neurodegeneration in PD.
摘要
线粒体是具有复杂结构特征的高度动态细胞器，它们发挥着多种重要的细胞功能，如通过氧化磷酸化产生能量、调节钙稳态或控制程序性细胞死亡 (PCD)。鉴于其在神经元存活中的重要作用，线粒体生物学的改变可导致神经元功能障碍和细胞死亡。线粒体呼吸缺陷一直被认为与帕金森病 (PD) 的病因和发病机制有关。然而，线粒体在 PD 中的作用远不止于呼吸缺陷，还涉及线粒体动力学的改变，导致线粒体形态、细胞内运输或质量控制的改变。线粒体功能障碍无论是原发性还是继发性事件，都有望成为一个潜在的治疗靶点，以阻止 PD 中多巴胺能神经退行性变的进展。
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2
Mitochondria: the next (neurode)generation.线粒体：下一代（神经）。
Neuron. 2011 Jun 23;70(6):1033-53. doi: 10.1016/j.neuron.2011.06.003.
3
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Nature. 2011 Jun 19;476(7360):336-40. doi: 10.1038/nature10230.
4
Mitochondria and programmed cell death in Parkinson's disease: apoptosis and beyond.帕金森病中的线粒体和程序性细胞死亡：细胞凋亡及其他。
Antioxid Redox Signal. 2012 May 1;16(9):883-95. doi: 10.1089/ars.2011.4074. Epub 2011 Jul 18.
5
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J Neurosci. 2011 May 11;31(19):7212-21. doi: 10.1523/JNEUROSCI.0711-11.2011.
6
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J Biol Chem. 2011 Jun 10;286(23):20710-26. doi: 10.1074/jbc.M110.213538. Epub 2011 Apr 13.
7
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J Biol Chem. 2011 May 6;286(18):16504-15. doi: 10.1074/jbc.M110.208447. Epub 2011 Mar 18.
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9
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10
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Nature. 2010 Dec 2;468(7324):696-700. doi: 10.1038/nature09536. Epub 2010 Nov 10.
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