神经退行性疾病中的内质网应激:从发病机制到治疗干预

IF 0.7
Felipe Cabral-Miranda, C. Hetz
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引用次数: 8

摘要

由错误折叠的蛋白质组成的蛋白质聚集体是几种神经退行性疾病发生的基础,这一概念表明这种现象可能有一个共同的起源,最终是由蛋白质平衡控制的破坏所驱动的。未折叠蛋白反应(UPR)是蛋白质静止网络的一个重要组成部分,该网络由内质网(ER)应激参与。慢性内质网应激可能是神经变性的一种可能机制,有助于突触改变、神经炎症和神经元丢失。在这篇综述中,我们讨论了内质网应激与不同神经退行性疾病发展的最新发现,以及可能的疾病干预策略。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
ER stress in neurodegenerative disease: from disease mechanisms to therapeutic interventions
Abstract The conception that protein aggregates composed by misfolded proteins underlies the occurrence of several neurodegenerative diseases suggests that this phenomenon may have a common origin, ultimately driven by disruption of proteostasis control. The unfolded protein response (UPR) embodies a major element of the proteostasis network, which is engaged by endoplasmic reticulum (ER) stress. Chronic ER stress may operate as a possible mechanism of neurodegeneration, contributing to synaptic alterations, neuroinflammation and neuronal loss. In this review we discuss most recent findings relating ER stress and the development of distinct neurodegenerative diseases, and the possible strategies for disease intervention.
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