{"title":"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","authors":"","doi":"10.1016/j.ibneur.2024.08.002","DOIUrl":null,"url":null,"abstract":"<div><p>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.</p></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":null,"pages":null},"PeriodicalIF":2.0000,"publicationDate":"2024-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S266724212400071X/pdfft?md5=2621e83bf9c81622baca20a8e1305936&pid=1-s2.0-S266724212400071X-main.pdf","citationCount":"0","resultStr":"{\"title\":\"Chemokines play a role in nerve damage and neuroprotection in vascular dementia\",\"authors\":\"\",\"doi\":\"10.1016/j.ibneur.2024.08.002\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><p>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.</p></div>\",\"PeriodicalId\":13195,\"journal\":{\"name\":\"IBRO Neuroscience Reports\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":2.0000,\"publicationDate\":\"2024-08-05\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.sciencedirect.com/science/article/pii/S266724212400071X/pdfft?md5=2621e83bf9c81622baca20a8e1305936&pid=1-s2.0-S266724212400071X-main.pdf\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"IBRO Neuroscience Reports\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S266724212400071X\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"NEUROSCIENCES\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"IBRO Neuroscience Reports","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S266724212400071X","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"NEUROSCIENCES","Score":null,"Total":0}
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.