趋化因子在血管性痴呆的神经损伤和神经保护中发挥作用

IF 2 Q3 NEUROSCIENCES
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引用次数: 0

摘要

各种趋化因子(FCs)在血管性痴呆的神经元损伤中发挥着不同的作用。CXCL5 和 CCL11 通过促进炎症反应加重神经损伤。CXCL13、XCL-1 和 CCL2/ MCP-1 在早期加重神经损伤,而在慢性进展期则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的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过程中起着重要作用。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,动态监测各种相关的趋化因子,了解趋化因子与小胶质细胞的关系,有助于了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证实,不同亚群的趋化因子与血管性痴呆密切相关。在临床研究中,上调 XCL-1 的新型免疫治疗方法和调节 CCL2/CCR2 信号通路活性的药物正在研究和推广之中。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Chemokines play a role in nerve damage and neuroprotection in vascular dementia

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.

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来源期刊
IBRO Neuroscience Reports
IBRO Neuroscience Reports Neuroscience-Neuroscience (all)
CiteScore
2.80
自引率
0.00%
发文量
99
审稿时长
14 weeks
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