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作 者:吴婧 施媛萍[1] WU Jing;SHI Yuanping(Clinical Medical Research Center,The Third Affiliated Hospital of Soochow University,Changzhou 213003,China)
机构地区:[1]苏州大学附属第三医院临床医学研究中心,江苏常州213003
出 处:《中国病理生理杂志》2023年第12期2288-2295,共8页Chinese Journal of Pathophysiology
基 金:分子发育生物学国家重点实验室开放课题(No.2022-MDB-KF-17);常州市国际科技合作计划(No.CZ20220024);常州市“十四五”卫生健康高层次人才培养工程拔尖人才(No.2022260)。
摘 要:在日常生活中,高血压、代谢综合征、吸烟和缺乏运动等条件可能诱发血管内皮细胞障碍^([1]),具体表现为内皮舒张功能受损、血管通透性增加、氧化应激和炎症等病理现象^([2]),正常内皮细胞的一个关键功能是防止血管黏附,内皮屏障异常导致内膜中形成包括各种细胞、脂质和组织碎屑在内的斑块,推动动脉粥样硬化的发展^([1])。Sphingosine-1-phosphate(S1P)is a bioactive lipid that regulates a variety of physiological processes,including immune surveillance,immune cell transport,vascular development,and cell differentiation.S1P also plays an important role in regulating vascular function and balancing endothelial barrier homeostasis.The majority of S1P molecules are located in their chaperone proteins,such as apolipoprotein M or albumin.The chaperone protein is also a carrier and modulator of S1P molecules,and the combination of the two can protect the S1P structure.S1P-binding chaperone protein selectively activates S1P receptor in the form of a complex that opens downstream pathways by coupling with different S1P receptor targets to exert its effects in vivo.The present review elucidates the metabolism and function of S1P,as well as the effect of chaperones on its function,and clarifies the regulation of S1P in vascular activity and pathogenesis of atherosclerosis.
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