神经退行性疾病和眼部疾病中的内质网-线粒体交叉对话

Neurology (E-Cronicon) Pub Date : 2019-09-01 Epub Date: 2019-08-29
Varun Kumar
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摘要

神经退行性疾病表现为大脑功能逐渐衰退,导致患者生活质量显著下降。随着预期寿命的延长,这些疾病的发病率也显著增加。阿尔茨海默氏症、帕金森氏症和肌萎缩性脊髓侧索硬化症等神经退行性疾病具有破坏性,困扰着全球众多人口。眼球与大脑的神经和血管相似,显示出其中一些神经疾病的许多病理特征。此外,这些疾病也给社会造成了经济和社会负担。尽管在药物研发方面做出了巨大努力,但这些致命疾病仍无法治愈。因此,了解这些疾病的细胞和分子病理生理学的需求尚未得到满足。所有这些疾病都会对大量看似不同的细胞过程和功能造成损害,如 Ca+2 稳态、脂质代谢、轴突运输、未折叠蛋白反应、自噬和炎症反应。线粒体与内质网(ER)密切相关,ER-线粒体之间的交叉对话调节着许多在神经退行性疾病和眼部疾病中受损的细胞过程和功能。一些研究表明,ER-线粒体接触的破坏与这些疾病有关。本综述旨在了解和总结ER-线粒体互作蛋白在迄今研究的主要神经退行性疾病和眼部疾病中的作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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Endoplasmic Reticulum-Mitochondrial Cross-Talk in Neurodegenerative and Eye Diseases.

Neurodegenerative diseases demonstrate the progressive decline of brain functions resulting in a significant deterioration in the quality of patient's life. With increasing life expectancy, there has been a significant increase in the incidence of these diseases. Neurodegenerative diseases like Alzheimer's, Parkinson's, and Amyotrophic lateral sclerosis are devastating and afflicts a large world population. Eye, given the similar neural and vascular similarity to the brain, demonstrates many pathological hallmarks of some of these neurological diseases. Moreover, these diseases create an economic and social burden to society. Despite tremendous efforts made in the drug discovery, there is no cure for these fatal diseases. Thus, there is an unmet need to understand cellular and molecular pathophysiology of these diseases. All these diseases demonstrate damage to a large number of seemingly disparate cellular processes and functions such as Ca+2 homeostasis, lipid metabolism, axonal transport, unfolded protein response, autophagy and inflammatory responses. Mitochondria are closely associated with Endoplasmic reticulum (ER) and ER-mitochondrial cross-talk regulates many of these cellular processes and functions damaged in neurodegenerative and eye diseases. Several studies have implicated the disruption of ER-mitochondria contacts in these diseases. This review is aimed at understanding and summarizing the role of ER-mitochondria interacting proteins in major neurodegenerative and eye diseases studied so far.

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