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CD4^(+)T淋巴细胞亚群与心肌梗死关系的研究进展

Research progress on the correlation between CD4^(+)T lymphocyte subsets and myocardial infarction
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摘要 心肌梗死(MI)是全球致死、致残的主要原因之一,严重危害人们的生命健康。进一步探索MI的相关病理机制有利于促进AMI的诊断、治疗和预后。MI设计复杂的病理过程,罪犯血管中往往含有大量可以诱导炎性反应的免疫细胞,其中以CD4^(+)T细胞亚群中的1型辅助性T(Th1)细胞最多见,此外还包括含量较低的Th2细胞、Th17细胞、调节性T细胞(Treg)、Th9细胞、Th22细胞及滤泡辅助性T(Tfh)细胞等。这些CD4^(+)T细胞通过自分泌或旁分泌方式释放多种细胞因子,并通过作用于炎性细胞调节动脉粥样硬化斑块的发生、发展。从而促进了MI的发生、发展,影响患者预后,本文就CD4^(+)T细胞亚群在MI的发生、发展、梗死后炎性反应及心室的不良重构等方面的研究进展进行综述,以期进一步阐明MI的病理过程,同时为MI预防、治疗及改善预后提供新的潜在靶点。 Myocardial infarction(MI)is one of the leading causes of death and disability worldwide,which seriously endangers the lives and health of people.A further exploration of the pathological mechanism of MI is conducive to the diagnosis,treatment and prognosis of acute MI(AMI).MI involves a complex pathological process.Criminal blood vessels often contain a large number of immune cells that can induce inflammation,among which type 1 helper T(Th1)cells in the CD4^(+)T cell subgroup are the most common ones.In addition,the contents of Th2 cells,Th17 cells,regulatory T cells(Treg),Th9 cells,Th22 cells and follicular auxiliary T(Tfh)cells realso low.These CD4^(+)T cells release a variety of cytokines through autocrine or paracrine mode and regulate the occurrence and development of atherosclerotic plaques by acting on inflammatory cells.Thus,it promotes the occurrence and development of MI and affects the prognosis of patients.This review summarized the research progress of CD4^(+)T cell subsets in the occurrence and development of MI,post-infarction inflammatory response and adverse ventricular remodeling,with a view to further elucidate the pathological process of MI and provide new potential targets for prevention,treatment and improvement of prognosis of MI.
作者 拓亚伟 任艳琴 高胜利 TUO Yawei;REN Yanqin;GAO Shengli(Fenyang College of Shanxi Medical University,Shanxi,Lvliang 032200,China;不详)
出处 《河北医药》 CAS 2024年第18期2848-2852,共5页 Hebei Medical Journal
基金 山西省卫生健康委科研课题(编号:2023017)。
关键词 心肌梗死 CD4^(+)T淋巴细胞亚群 辅助性T细胞 调节性T细胞 myocardial infarction CD4^(+)T lymphocyte subsets helper T cells regulatory T cells
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