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Fractalkine/CX3CR1 is involved in the cross-talk between neuron and glia in neurological diseases

•Described the activities of FKN, with either beneficial or detrimental effect.•Clarified the cross-talk of FKN/CX3CR1 between neurons and glial cells.•Summarized the mechanisms of FKN/CX3CR1 in brain-related diseases.•Discussed the potential clinical application of FKN. Fractalkine (CX3C chemokine...

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Bibliographic Details
Published in:Brain research bulletin 2019-03, Vol.146, p.12-21
Main Authors: Luo, Piao, Chu, Shi-feng, Zhang, Zhao, Xia, Cong-yuan, Chen, Nai-hong
Format: Article
Language:English
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Summary:•Described the activities of FKN, with either beneficial or detrimental effect.•Clarified the cross-talk of FKN/CX3CR1 between neurons and glial cells.•Summarized the mechanisms of FKN/CX3CR1 in brain-related diseases.•Discussed the potential clinical application of FKN. Fractalkine (CX3C chemokine ligand 1, CX3CL1) is an essential chemokine, for regulating adhesion and chemotaxis through binding to CX3CR1, which plays a critical role in the crosstalk between glial cells and neurons by direct or indirect ways in the central nervous system (CNS). Fractalkine/CX3CR1 axis regulates microglial activation and function, neuronal survival and synaptic function by controlling the release of inflammatory cytokines and synaptic plasticity in the course of the neurological disease. The multiple functions of fractalkine/CX3CR1 make it exert neuroprotective or neurotoxic effects, which determines the pathogenesis. However, the role of fractalkine/CX3CR1 in the CNS remains controversial. Whether it can be used as a therapeutic target for neurological diseases needs to be further investigated. In this review, we summarize the studies highlighting fractalkine/CX3CR1-mediated effects and discuss the potential neurotoxic and neuroprotective actions of fractalkine/CX3CR1 in brain injury for providing useful insights into the potential applications of fractalkine/CX3CR1 in neurological diseases.
ISSN:0361-9230
1873-2747
DOI:10.1016/j.brainresbull.2018.11.017