Targeting C-C Chemokine Receptor 5: Key to Opening the Neurorehabilitation Window After Ischemic Stroke.

Targeting C-C Chemokine Receptor 5: Key to Opening the Neurorehabilitation Window After Ischemic Stroke.
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靶向 C−C 趋化因子受体 5:缺血性中风后打开神经康复窗口的关键

DOI:
10.3389/fncel.2022.876342
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发表时间:
2022
影响因子:
5.3
通讯作者:
Wu, Qingping
Wu, Qingping
中科院分区:
医学2区
文献类型:
--
作者:
Feng, Yi-Qi;Xu, Zhen-Zhen;Wang, Yan-Ting;Xiong, Yue;Xie, Wanli;He, Yu-Yao;Chen, Lu;Liu, Guo-Yang;Li, Xia;Liu, Jie;Wu, Qingping

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中风是世界上第二大成人死亡和残疾原因,导致脑组织破坏和长期神经功能障碍;诱导神经元可塑性可促进中风后的恢复。C-C趋化因子受体5(CCR 5)可以指导白细胞迁移和定位,并且是可以介导人类免疫缺陷病毒(HIV)进入细胞的共受体。它在HIV感染和免疫应答中的作用已被广泛研究。此外,CCR 5在中枢神经系统(CNS)中广泛表达,参与各种生理活动,例如脑发育、神经元分化、通信、存活以及学习和记忆能力,并且还参与许多神经系统疾病的发展。CCR 5在中风后的神经元中差异性上调,并且在大脑的特定区域中抑制CCR 5促进运动和认知恢复。CCR 5作为治疗靶点促进脑卒中后神经康复的机制尚缺乏系统报道。本文就CCR 5在中枢神经系统中的功能及其通过调节神经可塑性和炎症反应影响脑卒中后恢复的机制进行综述,为脑卒中后的临床康复提供有效依据。
Stroke is the world’s second major cause of adult death and disability, resulting in the destruction of brain tissue and long-term neurological impairment; induction of neuronal plasticity can promote recovery after stroke. C–C chemokine receptor 5 (CCR5) can direct leukocyte migration and localization and is a co-receptor that can mediate human immunodeficiency virus (HIV) entry into cells. Its role in HIV infection and immune response has been extensively studied. Furthermore, CCR5 is widely expressed in the central nervous system (CNS), is engaged in various physiological activities such as brain development, neuronal differentiation, communication, survival, and learning and memory capabilities, and is also involved in the development of numerous neurological diseases. CCR5 is differentially upregulated in neurons after stroke, and the inhibition of CCR5 in specific regions of the brain promotes motor and cognitive recovery. The mechanism by which CCR5 acts as a therapeutic target to promote neurorehabilitation after stroke has rarely been systematically reported yet. Thus, this review aims to discuss the function of CCR5 in the CNS and the mechanism of its effect on post-stroke recovery by regulating neuroplasticity and the inflammatory response to provide an effective basis for clinical rehabilitation after stroke.
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