内质网应激与神经退行性疾病自噬的关系

IF 0.7
Toru Hosoi, J. Nomura, Keigo Tanaka, K. Ozawa, A. Nishi, Y. Nomura
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引用次数: 7

摘要

越来越多的证据表明,内质网应激和自噬在调节脑功能中起着重要作用。内质网应激激活了未折叠蛋白反应(UPR)途径的三个主要分支,即肌醇要求酶-1 (IRE1)、双链rna激活蛋白激酶(PKR)样内质网激酶(PERK)和激活转录因子6 (ATF6)介导的途径。最近的研究表明,这些UPR信号可能与自噬有关。在这篇综述文章中,我们总结了最近的证据,并讨论了内质网应激和神经退行性疾病中自噬之间的可能联系。此外,还讨论了针对UPR和自噬的可能的药理策略。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Link between endoplasmic reticulum stress and autophagy in neurodegenerative diseases
Abstract Increasing evidence suggests that endoplasmic reticulum (ER) stress and autophagy play an important role in regulating brain function. ER stress activates three major branches of the unfolded protein response (UPR) pathways, namely inositol-requiring enzyme-1 (IRE1), double stranded RNA-activated protein kinase (PKR)-like ER kinase (PERK) and activating transcription factor 6 (ATF6)-mediated pathways. Recent studies have suggested that these UPR signals may be linked to autophagy. In this review article, we summarize recent evidence and discuss a possible link between ER stress and autophagy with regard to neurodegenerative diseases. Furthermore, possible pharmacological strategies targeting UPR and autophagy are discussed.
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