内质网应激可能参与阿尔茨海默病的发病机制

IF 0.7
Toru Hosoi, J. Nomura, K. Ozawa, A. Nishi, Y. Nomura
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引用次数: 12

摘要

摘要内质网是一种在蛋白质折叠等蛋白质质量控制中起重要作用的细胞器。越来越多的证据表明内质网参与维持细胞稳态。然而,当细胞暴露于干扰内质网功能的应激条件时,未折叠的蛋白质积累导致内质网应激。然后细胞激活未折叠蛋白反应(UPR)来应对这种应激状态。在本综述中,我们将讨论和总结普遍定期审议基本机制的最新研究进展。我们还讨论了内质网应激在阿尔茨海默病(AD)发病机制中的可能参与。针对内质网应激的疾病的潜在治疗机会也被描述。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Possible involvement of endoplasmic reticulum stress in the pathogenesis of Alzheimer’s disease
Abstract The endoplasmic reticulum (ER) is an organelle that plays a crucial role in protein quality control such as protein folding. Evidence to indicate the involvement of ER in maintaining cellular homeostasis is increasing. However, when cells are exposed to stressful conditions, which perturb ER function, unfolded proteins accumulate leading to ER stress. Cells then activate the unfolded protein response (UPR) to cope with this stressful condition. In the present review, we will discuss and summarize recent advances in research on the basic mechanisms of the UPR. We also discuss the possible involvement of ER stress in the pathogenesis of Alzheimer’s disease (AD). Potential therapeutic opportunities for diseases targeting ER stress is also described.
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