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缺血性卒中后小胶质细胞极化机制与靶向治疗研究现状

Research satus of polarization mechanism and targeted therapy of microglia after ischemic stroke
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摘要 缺血性卒中(IS)后小胶质细胞极化机制研究近年取得重要进展,传统M1促炎/M2抗炎二分类模型已难以涵盖其复杂功能;单细胞转录组与空间转录组学研究证实,小胶质细胞存在亚群功能异质性及时空动态性。为阐明这些小胶质细胞亚群在IS中的作用并探讨潜在治疗靶点,本文围绕IS后小胶质细胞亚群的时空演变规律、分子调控网络特征、Toll样受体/髓样分化因子88/核因子-κB(TLRs/MYD88/NF-κB)、Janus激酶/信号转导与转录激活蛋白(JAK/STAT)等不同激活信号通路及以2型髓系细胞触发受体(TREM2)为代表的治疗靶点进行了阐述,以期为制定"分期、分区、分型"的靶向干预策略提供理论依据。 In recent years,significant progress has been made in studying polarization mechanism of microglia after ischemic stroke(IS).The traditional M1 pro-inflammatory/M2 anti-inflammatory dichotomy model is no longer sufficient to sum up the complex functions of microglia.Single-cell transcriptomics and spatial transcriptomics studies have confirmed that microglia subpopulations exhibit significant functional heterogeneity and spatiotemporal dynamics.To clarify the roles of these microglial subpopulations in IS and explore their potential therapeutic targets,this article elaborates on the spatiotemporal evolution patterns and molecular regulatory network characteristics of microglial subpopulations after IS,and their different activated signaling pathways such as Toll-like receptor/myeloid differentiation factor 88/nuclear factor-κB(TLRs/MYD88/NF-κB),Janus kinase/signal transducer and activator of transcription(JAK/STAT),and therapeutic targets represented by triggering receptor expressed on myeloid cells 2(TREM2),so as to provide a theoretical basis for formulating"phased,zoned,and typed"targeted intervention strategies.
作者 张鹏涛 贾琪 桑恩泽 黄庆锋 Zhang Pengtao;Jia Qi;Sang Enze;Huang Qingfeng(Department of Neurointervention,Affiliated Hospital of Nantong University,Nantong 226001,China)
出处 《中华神经医学杂志》 北大核心 2025年第12期1289-1295,共7页 Chinese Journal of Neuromedicine
关键词 缺血性卒中 小胶质细胞极化 功能异质性 时空动态性 2型髓系细胞触发受体 Ischemic stroke Microglial polarization Functional heterogeneity Spatiotemporal specificity Triggering receptor expressed on myeloid cells 2
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