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神经退行性变中的线粒体

Mitochondria in neurodegeneration.

作者信息

Chu Charleen T

机构信息

Departments of Pathology and Ophthalmology, Pittsburgh Institute for Neurodegenerative Diseases, McGowan Institute for Regenerative Medicine, Center for Protein Conformational Diseases, Center for Neuroscience at the University of Pittsburgh School of Medicine, Pittsburgh, PA 15261, USA.

出版信息

Curr Opin Physiol. 2022 Apr;26. doi: 10.1016/j.cophys.2022.100532. Epub 2022 Apr 1.

Abstract

The brain is one of the most energetically demanding tissues in the human body, and mitochondrial pathology is strongly implicated in chronic neurodegenerative diseases. In contrast to acute brain injuries in which bioenergetics and cell death play dominant roles, studies modeling familial neurodegeneration implicate a more complex and nuanced relationship involving the entire mitochondrial life cycle. Recent literature on mitochondrial mechanisms in Parkinson's disease, Alzheimer's disease, frontotemporal dementia, Huntington's disease, and amyotrophic lateral sclerosis is reviewed with an emphasis on mitochondrial quality control, transport and synaptodendritic calcium homeostasis. Potential neuroprotective interventions include targeting the mitochondrial kinase PTEN-induced kinase 1 (PINK1), which plays a role in regulating not only multiple facets of mitochondrial biology, but also neuronal morphogenesis and dendritic arborization.

摘要

大脑是人体中能量需求最高的组织之一,线粒体病理学与慢性神经退行性疾病密切相关。与生物能量学和细胞死亡起主导作用的急性脑损伤不同,模拟家族性神经退行性变的研究表明,整个线粒体生命周期存在更复杂、更细微的关系。本文综述了帕金森病、阿尔茨海默病、额颞叶痴呆、亨廷顿舞蹈病和肌萎缩侧索硬化中线粒体机制的最新文献,重点关注线粒体质量控制、运输和突触树突钙稳态。潜在的神经保护干预措施包括靶向线粒体激酶PTEN诱导激酶1(PINK1),它不仅在调节线粒体生物学的多个方面发挥作用,还在神经元形态发生和树突分支中发挥作用。

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Mitochondria in neurodegeneration.神经退行性变中的线粒体
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Activation mechanism of PINK1.PINK1 的激活机制。
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