抵抗素样分子在血管重塑中的作用及机制研究进展  

Advances in the role and mechanisms of resistin-like molecules in vascu⁃lar remodeling

作　　者：曹闲雅 谭骏岚 王飞英 戴爱国 CAO Xianya;TAN Junlan;WANG Feiying;DAI Aiguo(Department of Respiratory Diseases,Medical School,Hunan University of Chinese Medicine,Hunan Provincial Key Labo-ratory of Vascular Biology and Translational Medicine,Changsha 410208,China;Department of Respiratory Medicine,the First Affiliated Hospital,Hunan University of Chinese Medicine,Changsha 410021,China)

机构地区：[1]湖南中医药大学医学院呼吸疾病研究室,血管生物学与转化医学湖南省高校重点实验室,湖南长沙410208 [2]湖南中医药大学第一附属医院呼吸科,湖南长沙410021

出　　处：《中国病理生理杂志》2023年第6期1113-1120,共8页Chinese Journal of Pathophysiology

基　　金：国家自然科学基金资助项目(No.82200066);湖南省自然科学基金资助项目(No.2021JJ30017);湖南中医药大学中西医结合学院-明康中锦联合基金资助项目(No.2022MKZJ02)。

摘　　要：心血管疾病是全世界致残和死亡的首要因素,心血管疾病常伴随血管结构的改变[1]。越来越多的证据表明,血管重塑是心血管疾病和其他致死性疾病的病理基础。血管重塑会导致血管闭塞、狭窄、硬化、扩张甚至破裂,从而使血管正常生理功能发生障碍,引起众多疾病的发生[2]。Vascular remodeling is a prevalent pathological basis for many cardiovascular diseases.Therefore,understanding the regulatory mechanisms involved in vascular remodeling might provide insight into potential therapeutic targets and strategies for cardiovascular disease management.The family of resistin-like molecules(RELMs)consists mainly of four members in rodents such as RELMα/FIZZ1/HIMF,RELMβ/FIZZ2,resistin/FIZZ3,and RELMγ/FIZZ4.In humans,RELMs is composed of resistin and RELMβ.Notably,RELMs possess inflammatory regulating,chemokine,and growth factor properties and play an essential role in many pathophysiological processes.Recently,RELMs have been found to participate in vascular remodeling by regulating vascular cell proliferation,vascular smooth muscle cell phenotype transformation,extracellular matrix remodeling,angiogenesis,endothelial mesenchymal transformation,and inflammatory responses.The present paper reviews the role and mechanism of RELMs in vascular remodeling,aiming to provide a reference for the treatment of vascular remodeling-related diseases.

关 键 词：血管重塑 抵抗素样分子 血管平滑肌细胞 血管内皮细胞 

分 类 号：R363[医药卫生—病理学] R543[医药卫生—基础医学] R329.2