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缺血性卒中中的神经炎症:聚焦于微小RNA介导的小胶质细胞极化

Neuroinflammation in Ischemic Stroke: Focus on MicroRNA-mediated Polarization of Microglia.

作者信息

Lian Lu, Zhang Yunsha, Liu Lu, Yang Liji, Cai Yichen, Zhang Junping, Xu Shixin

机构信息

Medical Experiment Center, First Teaching Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin, China.

Tianjin Key Laboratory of Translational Research of TCM Prescription and Syndrome, Tianjin, China.

出版信息

Front Mol Neurosci. 2021 Jan 7;13:612439. doi: 10.3389/fnmol.2020.612439. eCollection 2020.

DOI:10.3389/fnmol.2020.612439
PMID:33488360
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7817943/
Abstract

Ischemic stroke is one of the most common causes of death and disability worldwide. Neuroinflammation is a major pathological event involved in the process of ischemic injury and repair. In particular, microglia play a dual role in neuroinflammation. During the acute phase of stroke onset, M2 microglia are the dominant phenotype and exert protective effects on neuronal cells, whereas permanent M1 microglia contribute to prolonged inflammation and are detrimental to brain tissue. Emerging evidence indicates that microRNAs (miRNAs) may have regulatory effects on microglia-associated inflammation. Thus, we briefly reviewed the dynamic response of microglia after a stroke and assessed how specific miRNAs affect the behavior of reactive microglia. We concluded that miRNAs may be useful novel therapeutic targets to improve stroke outcomes and modulate neuroinflammation.

摘要

缺血性中风是全球范围内死亡和残疾的最常见原因之一。神经炎症是缺血性损伤和修复过程中的一个主要病理事件。特别是,小胶质细胞在神经炎症中发挥双重作用。在中风发作的急性期,M2小胶质细胞是主要表型,对神经元细胞发挥保护作用,而持续存在的M1小胶质细胞会导致炎症延长,并对脑组织有害。新出现的证据表明,微小RNA(miRNA)可能对小胶质细胞相关炎症具有调节作用。因此,我们简要回顾了中风后小胶质细胞的动态反应,并评估了特定的miRNA如何影响反应性小胶质细胞的行为。我们得出结论,miRNA可能是改善中风预后和调节神经炎症的有用的新型治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c1ec/7817943/60ced3e39b1b/fnmol-13-612439-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c1ec/7817943/60ced3e39b1b/fnmol-13-612439-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c1ec/7817943/60ced3e39b1b/fnmol-13-612439-g0001.jpg

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