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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >From dysfunctional endoplasmic reticulum-mitochondria coupling to neurodegeneration
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From dysfunctional endoplasmic reticulum-mitochondria coupling to neurodegeneration

机译：来自功能失调的内质网 - 线粒体偶联至神经变性

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Abstract Over the last years, contact sites between the endoplasmic reticulum (ER) and mitochondria have attracted great attention in the study of cell homeostasis and dysfunction, especially in the context of neurodegenerative disorders. This is largely due to the critical involvement of this subcellular compartment in a plethora of vital cellular functions: Ca 2+ homeostasis, mitochondrial dynamics, transport, bioenergetics and turnover, ER stress, apoptotic signaling and inflammation. An increasing number of disease-associated proteins have been reported to physically associate with the ER-mitochondria interface, and cause structural and/or functional perturbations of this compartment. In the present review, we summarize current knowledge about the architecture and functions of the ER-mitochondria contact sites, and the consequences of their alteration in different neurodegenerative disorders. Special emphasis is placed on the caveats and difficulties in defining the nature and origin of the highlighted defects in ER-mitochondria communication, and their exact contribution to the neurodegenerative process. Highlights ? The ER-mitochondria interface is a multitasking subcellular platform regulating metabolism, membrane dynamics and signaling. ? Structural and functional defects of the ER-mitochondria interface are observed in neurodegenerative diseases. ? Defects in ER-mitochondria communication may reflect primary mechanisms, side-effects or compensatory responses. ? Combination of models and methodologies will help bypass current limitations in the study of ER-mitochondria contact sites.
机译：摘要在过去几年中，内质网（ER）和线粒体之间的接触地点在细胞稳态和功能障碍的研究中引起了极大的关注，特别是在神经变性障碍的背景下。这主要是由于这种亚细胞室在一个重要的蜂窝功能中的临界累及：Ca 2+稳态，线粒体动力学，运输，生物植物和周转，ER应激，凋亡信号传导和炎症。据报道，越来越多的疾病相关蛋白与ER-Mitochondria界面物理相关，并导致该隔室的结构和/或功能扰动。在本综述中，我们总结了关于ER-Mitochondria接触地点的架构和功能的现有知识，以及它们在不同神经变性障碍中改变的后果。特别强调在突出的突出显示缺陷在ER-Mitochondria通信中的突出显示的性质和起源以及对神经变性过程的确切贡献来说，特别强调。强调 ？ ER-Mitochondria界面是一个多任务亚细胞平台调节代谢，膜动力学和信号传导。还在神经变性疾病中观察到ER-Mitochondria界面的结构和功能缺陷。还ER-Mitochondria通信中的缺陷可能反映主要机制，副作用或补偿反应。还模型和方法的组合将有助于绕过ER-Mitochondria接触地点的电流限制。

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