脂质在自噬中的作用及其在神经变性中的意义。

IF 4.1 Q2 CELL BIOLOGY Cell Stress Pub Date : 2020-05-19 DOI:10.15698/cst2020.07.225
Sergio Hernandez-Diaz, Sandra-Fausia Soukup
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引用次数: 16

摘要

目前,神经退行性疾病在没有有效治疗的情况下是主要的社会经济负担,其日益流行意味着这些疾病将对子孙后代构成挑战。神经退行性疾病可能在病因和病理上有所不同,但通常是由功能失调和易聚集蛋白的积累引起的。自噬是一种保守的细胞机制,处理细胞应激和废物积累,并已被证明可以减少神经退行性疾病动物模型中功能失调蛋白的积累。从历史上看,对脂质精确功能的理解一直远远落后于其他生物分子(如蛋白质),但新兴的研究表明,脂质在自噬途径中的重要性,以及脂质代谢的紊乱如何与神经退行性变有关。在这里,我们回顾了改变的自噬和脂质代谢的紊乱,特别是磷酸肌醇和鞘脂,在神经退行性疾病中的特点,并介绍了该领域的工作,这些工作表明这些可能提供治疗干预的机会。
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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The role of lipids in autophagy and its implication in neurodegeneration.

Neurodegenerative diseases are, at present, major socio-economic burdens without effective treatments and their increasing prevalence means that these diseases will be a challenge for future generations. Neurodegenerative diseases may differ in etiology and pathology but are often caused by the accumulation of dysfunctional and aggregation-prone proteins. Autophagy, a conserved cellular mechanism, deals with cellular stress and waste product build-up and has been shown to reduce the accumulation of dysfunctional proteins in animal models of neurodegenerative diseases. Historically, progress in understanding the precise function of lipids has traditionally been far behind other biological molecules (like proteins) but emerging works demonstrate the importance of lipids in the autophagy pathway and how the disturbance of lipid metabolism is connected to neurodegeneration. Here we review how altered autophagy and the disturbance of lipid metabolism, particularly of phosphoinositols and sphingolipids, feature in neurodegenerative diseases and address work from the field that suggests that these potentially offer an opportunity of therapeutic intervention.

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来源期刊
Cell Stress
Cell Stress Biochemistry, Genetics and Molecular Biology-Biochemistry, Genetics and Molecular Biology (miscellaneous)
CiteScore
13.50
自引率
0.00%
发文量
21
审稿时长
15 weeks
期刊介绍: Cell Stress is an open-access, peer-reviewed journal that is dedicated to publishing highly relevant research in the field of cellular pathology. The journal focuses on advancing our understanding of the molecular, mechanistic, phenotypic, and other critical aspects that underpin cellular dysfunction and disease. It specifically aims to foster cell biology research that is applicable to a range of significant human diseases, including neurodegenerative disorders, myopathies, mitochondriopathies, infectious diseases, cancer, and pathological aging. The scope of Cell Stress is broad, welcoming submissions that represent a spectrum of research from fundamental to translational and clinical studies. The journal is a valuable resource for scientists, educators, and policymakers worldwide, as well as for any individual with an interest in cellular pathology. It serves as a platform for the dissemination of research findings that are instrumental in the investigation, classification, diagnosis, and therapeutic management of major diseases. By being open-access, Cell Stress ensures that its content is freely available to a global audience, thereby promoting international scientific collaboration and accelerating the exchange of knowledge within the research community.
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