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线粒体动态和神经退行性变中的乙酰化。

Acetylation in Mitochondria Dynamics and Neurodegeneration.

机构信息

Department of Pediatrics, University of Maryland School of Medicine, Baltimore, MD 21201, USA.

Veterans Affairs Maryland Health Center System, 10 North Greene Street, Baltimore, MD 21201, USA.

出版信息

Cells. 2021 Nov 5;10(11):3031. doi: 10.3390/cells10113031.

DOI:10.3390/cells10113031
PMID:34831252
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8616140/
Abstract

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.

摘要

线粒体由于其进化起源和在整体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,线粒体是主动移动、分裂或融合的。线粒体动力学过程由一组特定的蛋白质及其复杂的翻译后修饰来精细调节。在这篇综述中,我们讨论了线粒体动力学调节酶、它们的衔接蛋白以及乙酰化对融合和分裂机制活性的影响,这是对代谢应激的普遍反应。此外,我们还讨论了细胞内细胞骨架结构及其翻译后修饰在调节线粒体融合和分裂中的作用。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 依赖性去乙酰化调节的治疗策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/10f0/8616140/d8ba1193eaff/cells-10-03031-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/10f0/8616140/d7354484100c/cells-10-03031-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/10f0/8616140/05e4b6fb4ae8/cells-10-03031-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/10f0/8616140/d8ba1193eaff/cells-10-03031-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/10f0/8616140/d7354484100c/cells-10-03031-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/10f0/8616140/05e4b6fb4ae8/cells-10-03031-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/10f0/8616140/d8ba1193eaff/cells-10-03031-g003.jpg

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Cardioprotective role of SIRT1 activation on mitochondrial function in insulin-resistant H9c2 cells.SIRT1激活对胰岛素抵抗H9c2细胞线粒体功能的心脏保护作用。
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