低氧诱导因子在主动脉瘤形成中的作用  

Roles of hypoxia-inducible factors in aortic aneurysm formation

作　　者：刘欣如 马雨涛 于宝琪 曲爱娟[1,2] LIU Xin-ru;MA Yu-tao;YU Bao-qi;QU Ai-juan(Department of Physiology and Pathophysiology,School of Basic Medical Sciences,Capital Medical University,Beijing 100069,China;Key Laboratory of Remodeling-Related Cardiovascular Diseases,Ministry of Education,Capital Medical University,Beijing 100069,China)

机构地区：[1]首都医科大学基础医学院生理学与病理生理学系,北京100069 [2]首都医科大学重塑相关心血管疾病教育部重点实验室,北京100069

出　　处：《中国病理生理杂志》2021年第5期939-944,共6页Chinese Journal of Pathophysiology

基　　金：国家自然科学基金资助项目(No.81870186,No.91739120);北京市自然科学基金B类重点项目(No.KZ201910025027);北京市属高校高水平教师队伍建设支持计划青年拔尖人才项目(No.CIT&TCD201904090)。

摘　　要：1主动脉瘤概述主动脉瘤(aortic aneurysm,AA)通常被定义为主动脉直径≥30 mm的永久性和不可逆的血管局部扩张[1]。根据病灶部位的不同,主动脉瘤可分为扩张位于膈肌以下的腹主动脉瘤(abdominal aortic an-eurysm,AAA)和膈肌以上的胸主动脉瘤(thoracicaortic aneurysm,TAA)[2]。AA具有高发病率与高死亡率。近20年来,AAA在60岁以上男性发病率在4%~7.6%[3],TAA每年10.4人/10万人[2],在中国AAA破裂导致的死亡率高达80%以上[4]。Aortic aneurysm(AA)is an age-related life-threatening vascular disease usually managed by sur-gery or endovascular repair,and ruptured aneurysm has a mortality rate of over 80%. Although advances in the pathogene-sis of AA,such as extracellular matrix changes,smooth muscle cell loss,inflammatory cell infiltration,and increased oxi-dative stress,have largely broadened our knowledge of AA,the critical link between these pathophysiological mechanisms and druggable targets still remain elusive. In recent years,it is reported that hypoxia exists in AA. Hypoxia-inducible fac-tors(HIFs),as the central transcription factors for cellular adaptive responses to hypoxia,have been identified in the con-trol of numerous genes critical for multiple processes of AA,such as elastic fiber degradation,inflammation and angiogene-sis. This article aims to review these various proposed cellular mechanisms responsible for the involvement of hypoxia and HIFs in the formation and development of AA and to identify opportunities for future studies.

关 键 词：主动脉瘤 低氧诱导因子 血管平滑肌细胞 细胞外基质 炎症 血管新生 

分 类 号：R363.2[医药卫生—病理学] R543.16[医药卫生—基础医学]