脑卒中后神经炎症的小胶质细胞极化和治疗策略。

IF 4.8 3区医学 Q1 CLINICAL NEUROLOGY

Neurology and Therapy Pub Date : 2025-09-19 DOI:10.1007/s40120-025-00825-8

Travis Yui Hei Chan, Brian De Yu Ma, Timothy Keith Hung, Jenny Sum Yee Wong, Benjamin Wai Yue Lo

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引用次数: 0

摘要

中风仍然是全球致残的主要原因，由于不适应的神经炎症导致继发性损伤和损害恢复。早期的修复（M2）状态在几天内迅速转变为显性的破坏性（M1）表型，通过细胞因子[肿瘤坏死因子α (TNFα)，白细胞介素6 (IL-6)]的释放，血脑屏障破坏和外周免疫细胞浸润的扩大而加剧组织损伤。新兴的药物干预，如自由基清除剂依达拉奉、神经营养因子脑溶血素和兴奋毒性调节剂胞胆碱，在适当的时机显示出有希望的神经保护潜力。此外，新的非药物方法，包括重复经颅磁刺激、干细胞治疗和基于纳米颗粒的药物递送，为靶向神经炎症提供了创新的途径。然而，翻译方面的挑战仍然存在，包括狭窄的治疗窗口、生物标志物异质性和临床前与临床之间的差距。未来的进展需要整合时空药物递送、生物标志物引导的干预时机以及针对急性损伤和慢性修复阶段的协同组合方案的精准医学范式。通过将机制见解与临床应用相结合，本综述将神经炎症调节描述为重新定义卒中恢复的关键前沿，同时概述了克服现有障碍的基本研究轨迹。对PubMed、Web of Science、Embase和Cochrane（1996-2025）等电子数据库进行系统检索，使用PRISMA指南对符合条件的研究进行评估。通过专题分析，对缺血性脑卒中的神经炎症、机制或干预措施的研究结果进行了叙述性的综合。这篇综述总结了目前对脑卒中后神经炎症机制的见解，重点是小胶质细胞极化的双重作用。

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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Microglial Polarization and Therapeutic Strategies in Post-stroke Neuroinflammation.

Stroke remains a leading cause of global disability, perpetuated by maladaptive neuroinflammation that drives secondary injury and impairs recovery. An early reparative (M2) state rapidly transitions into a dominant destructive (M1) phenotype within days, worsening tissue damage through the release of cytokines [tumor necrosis factor alpha (TNFα), interleukin-6 (IL-6)], blood-brain barrier disruption, and amplified peripheral immune cell infiltration. Emerging pharmacological interventions, such as the free radical scavenger edaravone, the neurotrophic factor cerebrolysin, and the excitotoxicity modulator citicoline, demonstrate promising neuroprotective potential when strategically timed. Additionally, novel non-pharmacological approaches, including repetitive transcranial magnetic stimulation, stem cell therapy, and nanoparticle-based drug delivery, offer innovative pathways for targeting neuroinflammation. However, translational challenges persist, including narrow therapeutic windows, biomarker heterogeneity, and preclinical-to-clinical gaps. Future progress necessitates precision medicine paradigms integrating spatiotemporal drug delivery, biomarker-guided intervention timing, and synergistic combinatorial regimens targeting acute injury and chronic repair phases. By bridging mechanistic insights with clinical applications, this review delineates neuroinflammatory modulation as a pivotal frontier for redefining stroke recovery while outlining essential research trajectories to overcome existing barriers. Systematic search of electronic databases including PubMed, Web of Science, Embase, and Cochrane (1996-2025) was performed, with eligible studies assessed using PRISMA guidelines. Findings on neuroinflammation, mechanism, or interventions in ischemic stroke were narratively synthesized through thematic analysis. This review summarizes current insights into post-stroke neuroinflammatory mechanisms, with a focus on the dual role of microglial polarization.

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来源期刊

Neurology and Therapy CLINICAL NEUROLOGY-

CiteScore

5.40

自引率

8.10%

发文量

103

审稿时长

6 weeks

期刊介绍： Aims and Scope Neurology and Therapy aims to provide reliable and inclusive, rapid publication for all therapy related research for neurological indications, supporting the timely dissemination of research with a global reach, to help advance scientific discovery and support clinical practice. Neurology and Therapy is an international, open access, peer reviewed, rapid publication journal dedicated to the publication of high-quality clinical (all phases), observational, real-world and health outcomes research around the discovery, development, and use of neurological and psychiatric therapies, (also covering surgery and devices). Studies relating to diagnosis, pharmacoeconomics, public health, quality of life, and patient care, management, and education are also welcomed. The journal is of interest to a broad audience of healthcare professionals and publishes original research, reviews, case reports, trial designs, communications and letters. 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