Ma Jinming, Zhang Manqing, Fu Peijie, Yin Xiaoping, Chen Zhiying
Department of Neurology, Affiliated Hospital of Jiujiang University, Jiujiang,Jiangxi, 332000, China.
School of Basic Medicine, Jiujiang University, Jiujiang, Jiangxi, 332000, China.
IBRO Neurosci Rep. 2024 Aug 5;17:154-160. doi: 10.1016/j.ibneur.2024.08.002. eCollection 2024 Dec.
Various Chemotactic Factors (FCs) play different roles in neuronal injury in vascular dementia. CXCL5 and CCL11 exacerbate neurological injury by promoting inflammatory responses. CXCL12/SDF-1 and CX3CL1 play neuroprotective roles.CXCL13, XCL-1 and CCL2/ MCP-1 exacerbate neurological injury in the early stage, while exerting neuronal regeneration and neuroprotective effects in the chronic progressive phase. Chemokines often play an important role in the course of vascular dementia by regulating inflammatory responses, oxidative stress, and autophagy. Activation of microglia plays an important role in the regression of vascular dementia. Activated microglia M1 causes neuronal damage through the release of chemokines. And microglia M2 has anti-inflammatory effects and is involved in the repair of brain damage. Therefore, dynamic monitoring of various related FCs and understanding the relationship between FCs and microglia can help to understand and regulate the disease course progression of vascular dementia.At present, many scholars have confirmed in basic research that different subgroups of chemokines are closely related to vascular dementia. In clinical research, new immunotherapy methods that upregulate XCL-1 and drugs that regulate the activity of CCL2/CCR2 signaling pathways are being studied and promoted.
多种趋化因子(FCs)在血管性痴呆的神经元损伤中发挥着不同作用。CXCL5和CCL11通过促进炎症反应加剧神经损伤。CXCL12/SDF-1和CX3CL1发挥神经保护作用。CXCL13、XCL-1和CCL2/MCP-1在早期加剧神经损伤,而在慢性进展期发挥神经元再生和神经保护作用。趋化因子通常通过调节炎症反应、氧化应激和自噬在血管性痴呆病程中发挥重要作用。小胶质细胞的激活在血管性痴呆的消退中起重要作用。激活的小胶质细胞M1通过释放趋化因子导致神经元损伤。而小胶质细胞M2具有抗炎作用,并参与脑损伤的修复。因此,动态监测各种相关FCs并了解FCs与小胶质细胞之间的关系有助于理解和调控血管性痴呆的病程进展。目前,许多学者在基础研究中已证实趋化因子的不同亚组与血管性痴呆密切相关。在临床研究中,上调XCL-1的新免疫治疗方法以及调节CCL2/CCR2信号通路活性的药物正在研究和推广中。