趋化因子CX3CL1和受体CX3CR1在中枢神经系统疾病中的进展

Progress of CX3CL1(Fractalkine)and its receptor CX3CR1 in regulating central nervous system disease

越来越多的研究显示帕金森病、阿尔茨海默病、多发性硬化症等中枢神经系统疾病的发生可能和中枢神经系统炎症有关。趋化因子CX3CL1主要由神经元产生,作用于中枢神经系统,其与受体CX3CR1结合后可通过抑制神经元中的N-甲基-d-天冬氨酸受体(NMDA)诱导的钙内流,促进蛋白激酶的活化以及激活核转录因子кB,减少了炎症因子的释放,以及稳定小胶质细胞的状态,从而抑制中枢神经系统的炎症反应和减少神经元的死亡,起到一定的神经保护作用。因此,趋化因子CX3CL1与其受体CX3CR1的相互作用有望成为治疗中枢神经系统疾病的新靶点。文章就趋化因子CX3CL1与其受体CX3CR1的结构、相互作用的信号轴以及其在中枢神经系统疾病的研究进展进行综述。

In recent years,researches constituted to show that the occurrence of central nervous system diseases such as Parkinson′s disease,Alzheimer′s disease and multiple sclerosis may have association with the inflammation of central nervous system.The chemokine CX3CL1 is mainly produced by neurons and acts on the central nervous system.After binding to the receptor CX3CR1,by inhibiting the calcium influx induced by NMDA in neurons,it can promote the activation of protein kinase and activate nuclear transcription factor kappa B,reduce the release of inflammatory factors,and stabilize the status of microglia,thus suppress the inflammatory response of the central nervous system and reduce neuronal death,which play a certain role in neuroprotective effect.Therefore,the interaction between CX3CL1 and CX3CR1 is expected to be a new target in the treatment of central nervous system diseases.In this paper,the structure of CX3CL1 and its receptor CX3CR1,the interaction of signal axis and their research progress on central nervous system diseases are reviewed.