• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

E3泛素连接酶在脑缺血再灌注损伤中的作用

The Roles of E3 Ubiquitin Ligases in Cerebral Ischemia-Reperfusion Injury.

作者信息

Li Man, Yu Xiaoxiao, Liu Qiang, Fang Zhi, Wang Haijun

机构信息

Department of Neurology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.

Department of Neurosurgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.

出版信息

Int J Mol Sci. 2025 Jul 13;26(14):6723. doi: 10.3390/ijms26146723.

DOI:10.3390/ijms26146723
PMID:40724973
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12295222/
Abstract

The temporary or permanent occlusion of cerebral blood vessels results in ischemic stroke (IS). Ischemia per se causes focal neuronal damage, and the subsequent ischemia-reperfusion injury that occurs after blood flow restoration further compromises brain tissue and cells in the neurovascular unit, significantly contributing to poor patient outcomes and functional impairments. Current research indicates that the ubiquitin-proteasome system (UPS) plays a crucial role in the pathological processes associated with cerebral ischemia-reperfusion injury (CIRI). Notably, E3 ubiquitin (Ub) ligases, which are essential in the UPS, have garnered increasing attention as potential novel therapeutic targets for treating ischemia-reperfusion damage in the brain. This review focuses primarily on the background of E3 Ub ligases and explores their intricate relationships with the pathological processes of CIRI.

摘要

脑血管的暂时或永久性闭塞会导致缺血性中风(IS)。缺血本身会导致局灶性神经元损伤,而血流恢复后发生的后续缺血再灌注损伤会进一步损害神经血管单元中的脑组织和细胞,这对患者预后不良和功能障碍有显著影响。目前的研究表明,泛素-蛋白酶体系统(UPS)在与脑缺血再灌注损伤(CIRI)相关的病理过程中起关键作用。值得注意的是,作为UPS重要组成部分的E3泛素(Ub)连接酶,作为治疗脑缺血再灌注损伤的潜在新型治疗靶点,已受到越来越多的关注。本综述主要聚焦于E3 Ub连接酶的背景,并探讨它们与CIRI病理过程的复杂关系。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/00c7/12295222/0a95bcf4d2bc/ijms-26-06723-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/00c7/12295222/166d61a9d201/ijms-26-06723-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/00c7/12295222/08a47cb21881/ijms-26-06723-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/00c7/12295222/0a95bcf4d2bc/ijms-26-06723-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/00c7/12295222/166d61a9d201/ijms-26-06723-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/00c7/12295222/08a47cb21881/ijms-26-06723-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/00c7/12295222/0a95bcf4d2bc/ijms-26-06723-g003.jpg

相似文献

1
The Roles of E3 Ubiquitin Ligases in Cerebral Ischemia-Reperfusion Injury.E3泛素连接酶在脑缺血再灌注损伤中的作用
Int J Mol Sci. 2025 Jul 13;26(14):6723. doi: 10.3390/ijms26146723.
2
Beta-asarone alleviated cerebral ischemia/reperfusion injury by targeting PINK1/Parkin-dependent mitophagy.β-细辛醚通过靶向PINK1/帕金蛋白依赖性线粒体自噬减轻脑缺血/再灌注损伤。
Eur J Pharmacol. 2025 Sep 5;1002:177831. doi: 10.1016/j.ejphar.2025.177831. Epub 2025 Jun 7.
3
Deciphering the neuroprotective mechanisms of RACK1 in cerebral ischemia-reperfusion injury: Pioneering insights into mitochondrial autophagy and the PINK1/Parkin axis.解析 RACK1 在脑缺血再灌注损伤中的神经保护机制:对线粒体自噬和 PINK1/Parkin 轴的开创性见解。
CNS Neurosci Ther. 2024 Aug;30(8):e14836. doi: 10.1111/cns.14836.
4
E3 Ubiquitin Ligase Ring Finger Protein 2 Alleviates Cerebral Ischemia-Reperfusion Injury by Stabilizing Mesencephalic Astrocyte-Derived Neurotrophic Factor Through Monoubiquitination.E3 泛素连接酶环指蛋白 2 通过单泛素化稳定脑源性神经营养因子减轻脑缺血再灌注损伤。
CNS Neurosci Ther. 2024 Nov;30(11):e70136. doi: 10.1111/cns.70136.
5
Remote Ischemic Postconditioning Improve Cerebral Ischemia-Reperfusion Injury Induced Cognitive Dysfunction through Suppressing Mitochondrial Apoptosis in Hippocampus via TK/BK/B2R-Mediated PI3K/AKT.远程缺血后处理通过TK/BK/B2R介导的PI3K/AKT抑制海马体中的线粒体凋亡,改善脑缺血再灌注损伤所致的认知功能障碍。
Mol Neurobiol. 2025 Apr 14. doi: 10.1007/s12035-025-04864-y.
6
A systematic review of the research progress of non-coding RNA in neuroinflammation and immune regulation in cerebral infarction/ischemia-reperfusion injury.非编码 RNA 在脑梗死/缺血再灌注损伤中的神经炎症和免疫调节研究进展的系统评价。
Front Immunol. 2022 Oct 7;13:930171. doi: 10.3389/fimmu.2022.930171. eCollection 2022.
7
MiR-125a-5p in extracellular vesicles of neural stem cells acts as a crosstalk signal modulating neuroinflammatory microenvironment to alleviate cerebral ischemia-reperfusion injury.神经干细胞细胞外囊泡中的MiR-125a-5p作为一种串扰信号,调节神经炎症微环境以减轻脑缺血再灌注损伤。
Theranostics. 2025 Jun 12;15(14):7064-7089. doi: 10.7150/thno.115993. eCollection 2025.
8
Puerarin Alleviates Cerebral Ischemia-Reperfusion Injury by Inhibiting Ferroptosis Through SLC7A11/GPX4/ACSL4 Axis and Alleviate Pyroptosis Through Caspase-1/GSDMD Axis.葛根素通过SLC7A11/GPX4/ACSL4轴抑制铁死亡减轻脑缺血再灌注损伤,并通过半胱天冬酶-1/GSDMD轴减轻细胞焦亡。
Mol Neurobiol. 2025 Mar 8. doi: 10.1007/s12035-025-04798-5.
9
Enforced hematopoietic cell E-selectin/L-selectin ligand expression enhances bone marrow stromal cells homing and amelioration of cerebral ischemia-reperfusion injury via induction of prostaglandin E2.强制造血细胞E-选择素/L-选择素配体表达通过诱导前列腺素E2增强骨髓基质细胞归巢并改善脑缺血再灌注损伤。
Stem Cells. 2024 Dec 6;42(12):1070-1084. doi: 10.1093/stmcls/sxae062.
10
Protection of Dipsacoside B Against Cerebral Ischemia/Reperfusion Injury via Activating PINK1/Parkin-Mediated Mitophagy.通过激活PINK1/Parkin介导的线粒体自噬,双糖苷B对脑缺血/再灌注损伤的保护作用
J Biochem Mol Toxicol. 2025 Aug;39(8):e70416. doi: 10.1002/jbt.70416.

本文引用的文献

1
F-box proteins at the crossroads of ubiquitination and tumor immunity: regulatory networks and immunotherapy strategies.泛素化与肿瘤免疫交叉点上的F-box蛋白:调控网络与免疫治疗策略
Front Immunol. 2025 Jun 4;16:1596344. doi: 10.3389/fimmu.2025.1596344. eCollection 2025.
2
Research progress of deubiquitinating enzymes in cerebral ischemia-reperfusion injury.去泛素化酶在脑缺血再灌注损伤中的研究进展
Front Aging Neurosci. 2025 Jun 2;17:1588920. doi: 10.3389/fnagi.2025.1588920. eCollection 2025.
3
Emerging roles for E3 ubiquitin ligases in neural development and disease.
E3泛素连接酶在神经发育和疾病中的新作用。
Front Cell Dev Biol. 2025 May 27;13:1557653. doi: 10.3389/fcell.2025.1557653. eCollection 2025.
4
TRIM proteins: A 'swiss army knife' of antiviral immunity.TRIM蛋白:抗病毒免疫的“瑞士军刀”。
PLoS Pathog. 2025 May 12;21(5):e1013147. doi: 10.1371/journal.ppat.1013147. eCollection 2025 May.
5
Elucidating the immunomodulatory roles and mechanisms of CUL4B in the immune system: a comprehensive review.阐明CUL4B在免疫系统中的免疫调节作用及机制:一项综合综述
Front Immunol. 2025 Mar 31;16:1473817. doi: 10.3389/fimmu.2025.1473817. eCollection 2025.
6
Unraveling the Roles of UBE3A in Neurodevelopment and Neurodegeneration.揭示泛素蛋白连接酶E3A在神经发育和神经退行性变中的作用
Int J Mol Sci. 2025 Mar 5;26(5):2304. doi: 10.3390/ijms26052304.
7
Therapeutic potential of Parkin and its regulation in Parkinson's disease.Parkin 的治疗潜力及其在帕金森病中的调控。
Biochem Pharmacol. 2024 Dec;230(Pt 3):116600. doi: 10.1016/j.bcp.2024.116600. Epub 2024 Nov 3.
8
E3 ubiquitin ligase MARCH1 reduces inflammation and pyroptosis in cerebral ischemia-reperfusion injury via PCSK9 downregulation.E3 泛素连接酶 MARCH1 通过下调 PCSK9 减轻脑缺血再灌注损伤中的炎症和细胞焦亡。
Mamm Genome. 2024 Sep;35(3):346-361. doi: 10.1007/s00335-024-10055-2. Epub 2024 Aug 8.
9
Diversity of structure and function in Cullin E3 ligases.Cullin E3 连接酶的结构与功能多样性。
Curr Opin Struct Biol. 2024 Oct;88:102879. doi: 10.1016/j.sbi.2024.102879. Epub 2024 Jul 15.
10
Exploring the Role of Ubiquitin-Proteasome System in the Pathogenesis of Parkinson's Disease.探索泛素-蛋白酶体系统在帕金森病发病机制中的作用。
Pharmaceuticals (Basel). 2024 Jun 14;17(6):782. doi: 10.3390/ph17060782.