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脑白质损伤:蛛网膜下腔出血后治疗的新靶点

White Matter Injury: An Emerging Potential Target for Treatment after Subarachnoid Hemorrhage.

机构信息

Department of Neurosurgery, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang Province, China.

Key Laboratory of Precise Treatment and Clinical Translational Research of Neurological Diseases, Hangzhou, Zhejiang, China.

出版信息

Oxid Med Cell Longev. 2023 Feb 7;2023:3842493. doi: 10.1155/2023/3842493. eCollection 2023.

DOI:10.1155/2023/3842493
PMID:36798684
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9928519/
Abstract

Subarachnoid hemorrhage (SAH) refers to vascular brain injury mainly from a ruptured aneurysm, which has a high lifetime risk and imposes a substantial burden on patients, families, and society. Previous studies on SAH mainly focused on neurons in gray matter (GM). However, according to literature reports in recent years, in-depth research on the mechanism of white matter (WM) is of great significance to injury and recovery after SAH. In terms of functional recovery after SAH, all kinds of cells in the central nervous system (CNS) should be protected. In other words, it is necessary to protect not only GM but also WM, not only neurons but also glial cells and axons, and not only for the lesion itself but also for the prevention and treatment of remote damage. Clarifying the mechanism of white matter injury (WMI) and repair after SAH is of great importance. Therefore, this present review systematically summarizes the current research on WMI after SAH, which might provide therapeutic targets for treatment after SAH.

摘要

蛛网膜下腔出血 (SAH) 是指主要由破裂的动脉瘤引起的血管性脑损伤,具有很高的终生风险,给患者、家庭和社会带来了沉重的负担。先前关于 SAH 的研究主要集中在灰质 (GM) 的神经元上。然而,根据近年来的文献报道,深入研究白质 (WM) 的机制对于 SAH 后的损伤和恢复具有重要意义。就 SAH 后的功能恢复而言,中枢神经系统 (CNS) 中的各种细胞都需要得到保护。换句话说,不仅要保护 GM,还要保护 WM,不仅要保护神经元,还要保护神经胶质细胞和轴突,不仅要针对病变本身,还要针对远程损伤的预防和治疗。阐明 SAH 后 WM 损伤 (WMI) 的机制具有重要意义。因此,本综述系统总结了目前关于 SAH 后 WMI 的研究,这可能为 SAH 后的治疗提供治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9859/9928519/725fa3aa5880/OMCL2023-3842493.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9859/9928519/d6248fb98760/OMCL2023-3842493.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9859/9928519/2f6a8bb160f9/OMCL2023-3842493.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9859/9928519/725fa3aa5880/OMCL2023-3842493.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9859/9928519/d6248fb98760/OMCL2023-3842493.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9859/9928519/2f6a8bb160f9/OMCL2023-3842493.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9859/9928519/725fa3aa5880/OMCL2023-3842493.003.jpg

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EBioMedicine. 2022 Sep;83:104223. doi: 10.1016/j.ebiom.2022.104223. Epub 2022 Aug 13.
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Lipocalin-2-Mediated Insufficient Oligodendrocyte Progenitor Cell Remyelination for White Matter Injury After Subarachnoid Hemorrhage via SCL22A17 Receptor/Early Growth Response Protein 1 Signaling.脂联素-2 介导的少突胶质前体细胞再髓鞘化不足导致蛛网膜下腔出血后的白质损伤:通过 SCL22A17 受体/早期生长反应蛋白 1 信号通路。
Neurosci Bull. 2022 Dec;38(12):1457-1475. doi: 10.1007/s12264-022-00906-w. Epub 2022 Jul 7.
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消除 UCHL1 的水解酶活性会加剧小鼠缺血诱导的轴突损伤和功能缺陷。
J Cereb Blood Flow Metab. 2024 Nov;44(11):1349-1361. doi: 10.1177/0271678X241258809. Epub 2024 Jun 4.
White matter hyperintensity progression is associated with incident probable dementia or mild cognitive impairment.
白质高信号进展与新发的可能痴呆或轻度认知障碍相关。
Stroke Vasc Neurol. 2022 Apr 29;7(4):364-6. doi: 10.1136/svn-2021-001357.
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