| 摘要: |
| 脑卒中作为全球重大健康威胁,其发病机制与慢性炎症性血液病密切相关。系统性红斑狼疮和抗磷脂综合征等慢性炎症性血液病促进脑卒中发生的多维度机制。研究表明,慢性炎症性血液病通过多种相互关联的病理机制显著增加脑卒中风险,促炎细胞因子(如TNF-α和IL-6)不仅通过抑制紧密连接蛋白表达和激活NF-κB信号通路破坏血脑屏障完整性,还能激活小胶质细胞加重神经炎症反应；同时,活化的免疫细胞借助VCAM-1/ICAM-1介导的内皮黏附作用引发血管炎症并促进血栓形成；Notch1信号通路在外泌体转运的配体(DLL1/Jagged1)激活下加速动脉粥样硬化进程；此外,持续的炎症环境导致凝血-抗凝系统严重失衡,表现为组织因子表达上调、血小板异常活化、纤溶系统功能抑制以及弥散性血管内凝血(DIC)倾向,这些病理改变共同构成了 炎症-血管损伤-血栓形成 的恶性循环,最终显著提升脑卒中发生风险。本文旨在为深入解析慢性炎症性血液病相关脑卒中的病理机制提供新视角,对开发针对性预防策略和个体化治疗方案具有重要临床指导意义。 |
| 关键词: 脑卒中 信号通路 血管炎症 炎症反应 研究进展 |
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| 基金项目:]甘肃省重点研发计划(22YF7FA106)；甘肃省创新基地和人才计划(21JR7RA015)；联勤保障部队第九四〇医院血液病医学研究中心项目(2021yxky078) |
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| Research progress on the mechanism of chronic inflammatory hematological diseases in the pathogenesis of stroke |
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ZOU Caizu, ZHENG Ruirui, WEI Ailing, WEI Lixia, WEI Furong, XI Jingfei
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Department of Hematology,th Hospital of the Joint Logistics Support Force,Lanzhou,Gansu
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| Abstract: |
| Stroke is a major global health threat, and its pathogenesis is closely related to chronic inflammatory hematological diseases. The multi-dimensional mechanism of chronic inflammatory hematological diseases such as systemic lupus erythematosus and antiphospholipid syndrome promoting stroke. Studies have shown that chronic inflammatory hematological diseases significantly increase the risk of stroke through a variety of interrelated pathological mechanisms. Proinflammatory cytokines ( such as TNF-α and IL-6 ) not only destroy the integrity of the blood-brain barrier by inhibiting the expression of tight junction proteins and activating the NF-κB signaling pathway, but also activate microglia to aggravate the neuroinflammatory response. At the same time, activated immune cells trigger vascular inflammation and promote thrombosis by VCAM-1 / ICAM-1-mediated endothelial adhesion ; the Notch1 signaling pathway accelerates the process of atherosclerosis under the activation of exosome-transporting ligand ( DLL1 / Jagged1 ) ; in addition, the continuous inflammatory environment leads to a serious imbalance in the coagulation-anticoagulation system, manifested as up-regulation of tissue factor expression, abnormal platelet activation, inhibition of fibrinolytic system function, and tendency of disseminated intravascular coagulation ( DIC ). These pathological changes together constitute a vicious cycle of " inflammation-vascular injury-thrombosis ", which ultimately significantly increases the risk of stroke.This article aims to provide a new perspective for in-depth analysis of the pathological mechanism of stroke associated with chronic inflammatory hematological diseases, and has important clinical guiding significance for the development of targeted prevention strategies and individualized treatment options. |
| Key words: stroke signal pathway vascular inflammation inflammatory reaction research progress |