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缺血性中风后神经元中乙酰化介导的溶酶体与自噬体融合的机制。

The mechanism of acetylation-mediated fusion of lysosomes with autophagosomes in neurons after ischemic stroke.

作者信息

Yu Meilin, Xiong Yajie, He Hongyun, Deng Yihao

机构信息

School of Basic Medical Sciences, Kunming University of Science and Technology, Kunming 650500, China.

School of Basic Medical Sciences, Kunming University of Science and Technology, Kunming 650500, China.

出版信息

Life Sci. 2025 Feb 1;362:123305. doi: 10.1016/j.lfs.2024.123305. Epub 2024 Dec 7.

DOI:10.1016/j.lfs.2024.123305
PMID:39653133
Abstract

Ischemic stroke is a serious cerebrovascular disease that brings a significant threat to human health. Considerable factors are involved in occurrence of cerebral ischemia. Among them, autophagy is an important intracellular process that is activated after ischemic stroke, which plays a crucial role in maintaining homeostasis and survival of neurons. The fusion of lysosomes with autophagosomes is a key step in autophagic processes. In recent decades, investigations have found that acetylation, a common post-translational modification of proteins, has an important regulatory effect on autophagy. The present article focuses on elucidating mechanism and roles of acetylation in fusion of lysosomes with autophagosomes in neurons after ischemic stroke, to seek novel targets and strategies for deeper understanding of the pathogenesis of ischemic stroke. This review is also to provide clues for clinical treatment of ischemic stroke.

摘要

缺血性中风是一种严重的脑血管疾病,对人类健康构成重大威胁。脑缺血的发生涉及诸多因素。其中,自噬是缺血性中风后被激活的重要细胞内过程,在维持神经元的内环境稳定和存活中起关键作用。溶酶体与自噬体的融合是自噬过程中的关键步骤。近几十年来,研究发现乙酰化作为一种常见的蛋白质翻译后修饰,对自噬具有重要的调节作用。本文重点阐述缺血性中风后神经元中乙酰化在溶酶体与自噬体融合中的机制和作用,旨在寻找新的靶点和策略,以更深入地了解缺血性中风的发病机制。本综述还为缺血性中风的临床治疗提供线索。

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Life Sci. 2025 Feb 1;362:123305. doi: 10.1016/j.lfs.2024.123305. Epub 2024 Dec 7.
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