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.
复制标题
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
中科院分区:
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
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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