缺血性脑卒中后小胶质细胞极化中 RhoA/ROCK/NF-κB 通路的作用

IF 6.2
Weizhuo Lu, Yilin Wang, Jiyue Wen
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引用次数: 0

摘要

缺血性中风是导致全球死亡和残疾的主要原因。然而,缺血性中风仍然缺乏有效的治疗方法。小胶质细胞是中枢神经系统(CNS)的常驻巨噬细胞,可启动免疫反应并监测微环境。小胶质细胞在包括缺血性中风在内的各种脑损伤中被激活并极化为促炎或抗炎表型。促炎性小胶质细胞可产生免疫调节介质,包括细胞因子和趋化因子,这些介质与缺血性中风后的继发性脑损伤密切相关。相反,抗炎性小胶质细胞有助于中风后的恢复。调节小胶质细胞的活化和功能对于探索缺血性中风患者的新疗法至关重要。大量研究表明,RhoA/ROCK 通路和 NF-κB 是小胶质细胞活化和极化过程中的著名调节因子。抑制这些关键调节因子可促进小胶质细胞极化为抗炎表型。在这篇综述中,我们旨在全面概述 RhoA/ROCK 通路和 NF-κB 在小胶质细胞活化和极化过程中的作用,揭示 RhoA/ROCK 通路和 NF-κB 在缺血性卒中病理过程中的关系。此外,我们还讨论了针对小胶质细胞极化的药物调节剂。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

The Roles of RhoA/ROCK/NF-κB Pathway in Microglia Polarization Following Ischemic Stroke.

The Roles of RhoA/ROCK/NF-κB Pathway in Microglia Polarization Following Ischemic Stroke.

Ischemic stroke is the leading cause of death and disability worldwide. Nevertheless, there still lacks the effective therapies for ischemic stroke. Microglia are resident macrophages of the central nervous system (CNS) and can initiate immune responses and monitor the microenvironment. Microglia are activated and polarize into proinflammatory or anti‑inflammatory phenotype in response to various brain injuries, including ischemic stroke. Proinflammatory microglia could generate immunomodulatory mediators, containing cytokines and chemokines, these mediators are closely associated with secondary brain damage following ischemic stroke. On the contrary, anti-inflammatory microglia facilitate recovery following stroke. Regulating the activation and the function of microglia is crucial in exploring the novel treatments for ischemic stroke patients. Accumulating studies have revealed that RhoA/ROCK pathway and NF-κB are famous modulators in the process of microglia activation and polarization. Inhibiting these key modulators can promote the polarization of microglia to anti-inflammatory phenotype. In this review, we aimed to provide a comprehensive overview on the role of RhoA/ROCK pathway and NF-κB in the microglia activation and polarization, reveal the relationship between RhoA/ROCK pathway and NF-κB in the pathological process of ischemic stroke. In addition, we likewise discussed the drug modulators targeting microglia polarization.

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