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巨噬细胞在颅内动脉瘤发生发展中的作用研究进展
引用本文:王雅琪,金静华.巨噬细胞在颅内动脉瘤发生发展中的作用研究进展[J].浙江大学学报(医学版),2019,48(2):204-213.
作者姓名:王雅琪  金静华
作者单位:浙江大学医学院神经生物学系, 浙江 杭州 310058
基金项目:国家自然科学基金(81671131, 81171199);浙江省自然科学基金(LY19H090022)
摘    要:大量研究表明慢性炎性反应是颅内动脉瘤(IA)形成和破裂的核心环节,作为IA病变中最多见的炎症细胞,巨噬细胞通过多种途径调控IA的发生、发展。骨髓来源单核细胞分化而来的巨噬细胞及组织固有巨噬细胞浸润血管壁;浸润后的巨噬细胞受不同刺激极化为以M1型和M2型巨噬细胞为主的各类极化表型;各种极化表型的巨噬细胞既能通过释放细胞因子和调控其他免疫细胞调控炎性反应,也能释放不同细胞因子作用于细胞外基质重塑过程,从而调控颅内动脉瘤的发生、发展。临床上,以巨噬细胞为靶点的检测和治疗手段已取得一定进展。本文为深入理解IA发病机制和寻找阻止颅内动脉瘤形成和破裂的药物治疗提供理论依据。

关 键 词:巨噬细胞/病理学  颅内动脉瘤/病理学  炎症  肿瘤坏死因子α/分泌  基质金属蛋白酶类  免疫    细胞  核因子κB  
收稿时间:2018-11-20

Roles of macrophages in formation and progression of intracranial aneurysms
WANG Yaqi,JIN Jinghua.Roles of macrophages in formation and progression of intracranial aneurysms[J].Journal of Zhejiang University(Medical Sciences),2019,48(2):204-213.
Authors:WANG Yaqi  JIN Jinghua
Institution:Department of Neurobiology, Zhejiang University School of Medicine, Hangzhou 310058, China
Abstract:Studies have shown that chronic inflammatory response plays a key role in intracranial aneurysms (IA) formation and progression, and macrophages regulate the formation and progression of IA through a variety of pathways. Bone marrow monocyte-derived macrophages and resident-tissue macrophages infiltrate the vessel wall, after infiltration macrophages are polarized into various polarization phenotypes dominated by M1-like and M2-like cells. Polarized phenotypes of macrophages can regulate the formation and progression of intracranial aneurysms by releasing cytokines and regulating the inflammatory response of other immune cells, as well as release different cytokines to regulate the process of extracellular matrix remodeling. Some important progresses have been made in the clinical detection and treatment in targeting macrophages. This review provides a summary on the pathogenesis of IA and potential drug targets to prevent the formation and rupture of intracranial aneurysms.
Keywords:Macrophages/pathology  Intracranial aneurysm/pathology  Inflammation  Tumor necrosis factor-alpha/secretion  Matrix metalloproteinases  Immunity  cellular  Nuclear factor-kappa B  
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