淀粉样脑血管病相关铁代谢紊乱  

Dysregulation of iron metabolism in cerebral amyloid angiopathy

作　　者：叶晓东 李萍[1] 黄珊珊[1] 朱遂强[1] YE Xiao-dong;LI Ping;HUANG Shan-shan;ZHU Sui-qiang(Department of Neurology,Tongji Hospital,Tongji Medical College,Huazhong University of Science and Technology,Hubei Wuhan,430030,China)

机构地区：[1]华中科技大学同济医学院附属同济医院神经科,湖北武汉430030

出　　处：《内科急危重症杂志》2022年第3期182-185,共4页Journal of Critical Care In Internal Medicine

基　　金：湖北省技术创新专项(No:2019ACA132);华中科技大学自主创新项目(No:2019kfyXKJC075);华中科技大学同济医学院附属同济医院科研基金项目(No:2021B22)。

摘　　要：淀粉样脑血管病(CAA)是一种淀粉样蛋白(Aβ)沉积于皮质、皮质下小动脉及毛细血管的脑小血管病。中枢神经系统(CNS)的生理性铁代谢包括铁进入、代谢和清除过程。Aβ自身结构易结合铁导致铁积聚,Aβ沉积原位炎症相关星形胶质细胞活化、Aβ沉积血管壁继发血脑屏障破坏及出血性事件,如脑出血、非动脉瘤性蛛网膜下腔出血、微出血及皮质表面含铁血黄素沉积等,均可加剧CNS铁沉积、诱发CNS的铁代谢紊乱。同时,铁代谢紊乱诱导Aβ产生及毒性增加,继发氧化应激、神经炎症和铁死亡,从而加速血管损伤,推动CAA病理及临床事件演变。本综述旨在探讨CAA中的铁代谢紊乱,为CAA潜在可能临床治疗靶点提供依据。Cerebral amyloid angiopathy(CAA)is a type of cerebral small vessel disease with amyloid-β(Aβ)deposition on cortical or subcortical arterioles or capillaries.In the central nervous system(CNS),the entrance,metabolism and clearance of iron normally operate in a regular manner.The facilitation of Aβstructure binding to iron,the Aβdeposition mediating inflammation with reactive astrocyte and the Aβdeposition on cerebral vessel wall resulting in blood-brain barrier damage and hemorrhagic events,including intracerebral hemorrhage,non-aneurysmal subarachnoid hemorrhage,cerebral microbleeds or cortical superficial siderosis etc.,all conceivably drive the exceeded iron deposition and iron dysmetabolism in the CNS.Meanwhile,iron dysmetabolism can evoke the production and cytotoxicity of beta-amyloid,the process of oxidative stress,neuroinflammation and ferroptosis etc.,which all potentially contribute to the damage to cerebral vasculature and promote the progression on the pathophysiology and clinical characteristics of CAA.Our review will discuss the dysregulation of iron metabolism in CAA,aiming at providing fundamental evidence on potential treatments of CAA.

关 键 词：淀粉样脑血管病 铁代谢 Β-淀粉样蛋白 

分 类 号：R743[医药卫生—神经病学与精神病学]