Acetylation in Mitochondria Dynamics and Neurodegeneration.

Acetylation in Mitochondria Dynamics and Neurodegeneration.
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DOI:
10.3390/cells10113031
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发表时间:
2021-11-05
期刊:
影响因子:
6
通讯作者:
Kristian T
Kristian T
中科院分区:
生物学2区
文献类型:
--
作者:
Waddell J;Banerjee A;Kristian T

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线粒体因其进化起源和在整个细胞生理学和病理生理学中的多功能作用而成为一种独特的细胞内细胞器。为了满足细胞内特定的空间代谢需求,线粒体正在积极移动、分裂或融合。线粒体动力学的这一过程由一组特定的蛋白质及其复杂的翻译后修饰进行微调。在这篇综述中,我们讨论了线粒体动力学调节酶、它们的接头蛋白,以及乙酰化对融合和裂变机制活性的影响,作为对代谢应激的普遍反应。此外,我们讨论了细胞内细胞骨架结构及其翻译后修饰在线粒体融合和裂变调节中的作用。最后,我们回顾了线粒体动力学失调在急性脑损伤病理生理学中的作用以及基于 NAD+ 依赖性脱乙酰化调节的治疗策略。
Mitochondria are a unique intracellular organelle due to their evolutionary origin and multifunctional role in overall cellular physiology and pathophysiology. To meet the specific spatial metabolic demands within the cell, mitochondria are actively moving, dividing, or fusing. This process of mitochondrial dynamics is fine-tuned by a specific group of proteins and their complex post-translational modifications. In this review, we discuss the mitochondrial dynamics regulatory enzymes, their adaptor proteins, and the effect of acetylation on the activity of fusion and fission machinery as a ubiquitous response to metabolic stresses. Further, we discuss the role of intracellular cytoskeleton structures and their post-translational modifications in the modulation of mitochondrial fusion and fission. Finally, we review the role of mitochondrial dynamics dysregulation in the pathophysiology of acute brain injury and the treatment strategies based on modulation of NAD+-dependent deacetylation.
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