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作 者:彭勇[1,2] 高文月 秦娣 PENG Yong;GAO Wen-Yue;QIN Di(Jiangsu Collaborative Innovation Center for Sports and Health Project,Nanjing 210014,China;Key Laboratory of Human Sports Science for Jiangsu Province,Nanjing Sport Institute,Nanjing 210014,China;School of Sport Health,Nanjing Sport Institute,Nanjing 210014,China)
机构地区:[1]南京体育学院江苏省运动与健康工程协同创新中心,南京210014 [2]南京体育学院江苏省运动人体科学重点实验室,南京210014 [3]南京体育学院运动健康学院,南京210014
出 处:《生理学报》2025年第1期95-106,共12页Acta Physiologica Sinica
基 金:Natural Science Foundation of Jiangsu Province,China(No.20KJB310004);Jiangsu Provincial Sports and Health Engineering Collaborative Innovation Center Third Construction Phase Youth Project(No.JSCIC-YP21001);Jiangsu Provincial Qinglan Engineering Academic Leader Project Funding(2022);National College Student Innovation and Entrepreneurship Training Program Project(No.202310330001Z);Nanjing Sport University"1+1"Excellent Academic Team Project(No.XSTD202317)。
摘 要:本文综述了不同类型的T淋巴细胞亚群在心脏纤维化重构中的作用。辅助性T细胞17(T helper cell 17,Th17)参与促进心脏纤维化重构的发展,而调节性T细胞(regulatory T cell,Treg)作为负调节因子发挥免疫抑制功能,这归因于其分泌白介素-10(interleukin-10,IL-10)和功能表型。Th1和Th2细胞参与病理性心脏纤维化重构中炎症反应的不同阶段,这两类细胞的作用因不同心脏疾病的病理机制而异。此外,CD8+T细胞调节巨噬细胞的活化和极化,促进颗粒酶B的分泌,诱导心肌细胞凋亡,加重心肌梗死后的心脏纤维化。考虑到细胞因子调节在心力衰竭临床治疗中的局限性,靶向T细胞共刺激分子成为治疗病理性心脏重塑的一种有前景的策略。未来的研究将探索嵌合抗原受体修饰T细胞(chimeric antigen receptor modified T cells,CAR-T cells)技术和靶向调节Treg细胞数量与表型,二者具有成为心脏病有效疗法的潜力。This article reviews the role of different types of T lymphocyte subpopulations in pathological cardiac fibrosis remodeling.T helper 17(Th17)cells are implicated in promoting the development of pathological cardiac fibrosis remodeling,while regulatory T(Treg)cells exert an immunosuppressive functions as negative regulators,attributing to their interleukin-10(IL-10)secretion and functional phenotype.Th1 and Th2 cells are involved in different stages of the inflammatory response in pathological cardiac fibrosis remodeling,and their influence varies according to the pathological mechanisms of different cardiac diseases.In addition,CD8+T cells regulate the activation and polarization of macrophages,promote the secretion of granzyme B,induce cardiomyocyte apoptosis,and aggravate cardiac fibrosis post-myocardial infarction.Considering the limitation of cytokine modulation in clinical therapy of heart failure,targeting T-cell co-stimulatory molecules emerges as a promising strategy for treating pathologic cardiac remodeling.Future research will explore chimeric antigen receptor modified T cells(CAR-T cells)technology and targeted regulation of Treg cells quantity and phenotype,for both of which have the potential to become effective methods for treating heart disease.
分 类 号:R541.6[医药卫生—心血管疾病]
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