蛛网膜下腔出血后小胶质细胞的活化和极化

Z. Zheng, Kwok Chu George Wong
{"title":"蛛网膜下腔出血后小胶质细胞的活化和极化","authors":"Z. Zheng, Kwok Chu George Wong","doi":"10.20517/2347-8659.2018.52","DOIUrl":null,"url":null,"abstract":"Subarachnoid hemorrhage (SAH) is a devastating stroke type, with high mortality and morbidity. The neuroinflammatory response evolves over time from early brain injury to delayed cerebral deterioration. Microglia, the resident immune cells of the central nervous system, respond to the acute brain injury through activation and polarization. Microglia are able to polarize along two pathways, classic M1 and alternative M2, towards tissue injury and tissue repair respectively. The modulation of microglial activation has gained appreciation as a means to prevent the detrimental effects. In this review, we describe the progression of microglial polarization after SAH and summarize the key studies on mediators of microglial activation, including M1 and M2 specific microglial markers, transcription factors and key signaling pathways. Interactions between microglia and other cells are critical in modulating microglial activation and function, which are discussed as well. The preclinical application of microgliadependent treatments is presented, aiming for a better understanding of modulating microglial function and suggesting future investigation for therapeutic approaches.","PeriodicalId":19129,"journal":{"name":"Neuroimmunology and Neuroinflammation","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2019-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"24","resultStr":"{\"title\":\"Microglial activation and polarization after subarachnoid hemorrhage\",\"authors\":\"Z. Zheng, Kwok Chu George Wong\",\"doi\":\"10.20517/2347-8659.2018.52\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Subarachnoid hemorrhage (SAH) is a devastating stroke type, with high mortality and morbidity. The neuroinflammatory response evolves over time from early brain injury to delayed cerebral deterioration. Microglia, the resident immune cells of the central nervous system, respond to the acute brain injury through activation and polarization. Microglia are able to polarize along two pathways, classic M1 and alternative M2, towards tissue injury and tissue repair respectively. The modulation of microglial activation has gained appreciation as a means to prevent the detrimental effects. In this review, we describe the progression of microglial polarization after SAH and summarize the key studies on mediators of microglial activation, including M1 and M2 specific microglial markers, transcription factors and key signaling pathways. Interactions between microglia and other cells are critical in modulating microglial activation and function, which are discussed as well. The preclinical application of microgliadependent treatments is presented, aiming for a better understanding of modulating microglial function and suggesting future investigation for therapeutic approaches.\",\"PeriodicalId\":19129,\"journal\":{\"name\":\"Neuroimmunology and Neuroinflammation\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2019-01-14\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"24\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Neuroimmunology and Neuroinflammation\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.20517/2347-8659.2018.52\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Neuroimmunology and Neuroinflammation","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.20517/2347-8659.2018.52","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 24

摘要

蛛网膜下腔出血(SAH)是一种极具破坏性的中风类型,具有较高的死亡率和发病率。神经炎症反应随着时间的推移从早期脑损伤演变为延迟性脑退化。小胶质细胞是中枢神经系统的固有免疫细胞,通过激活和极化对急性脑损伤做出反应。小胶质细胞能够沿着两种途径极化,即经典的M1和替代的M2,分别朝向组织损伤和组织修复。小胶质细胞激活的调节作为一种防止有害影响的手段已经得到了重视。在这篇综述中,我们描述了SAH后小胶质细胞极化的进展,并总结了关于小胶质细胞激活介质的关键研究,包括M1和M2特异性小胶质细胞标记物、转录因子和关键信号通路。小胶质细胞和其他细胞之间的相互作用在调节小胶质细胞的激活和功能方面至关重要,这一点也进行了讨论。介绍了小胶质细胞依赖性治疗的临床前应用,旨在更好地了解调节小胶质细胞功能,并建议未来对治疗方法进行研究。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Microglial activation and polarization after subarachnoid hemorrhage
Subarachnoid hemorrhage (SAH) is a devastating stroke type, with high mortality and morbidity. The neuroinflammatory response evolves over time from early brain injury to delayed cerebral deterioration. Microglia, the resident immune cells of the central nervous system, respond to the acute brain injury through activation and polarization. Microglia are able to polarize along two pathways, classic M1 and alternative M2, towards tissue injury and tissue repair respectively. The modulation of microglial activation has gained appreciation as a means to prevent the detrimental effects. In this review, we describe the progression of microglial polarization after SAH and summarize the key studies on mediators of microglial activation, including M1 and M2 specific microglial markers, transcription factors and key signaling pathways. Interactions between microglia and other cells are critical in modulating microglial activation and function, which are discussed as well. The preclinical application of microgliadependent treatments is presented, aiming for a better understanding of modulating microglial function and suggesting future investigation for therapeutic approaches.
求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
自引率
0.00%
发文量
348
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信