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miR-363-5p和IL-34介导的调制心脏起器通道,HCN4,在iPSC-CM上:转化为人类鼻节微环境

Zeyuan Yin¹, Tong Fu², Lu Fu³

¹Cardiovascular Sciences, Faculty of Biology, Medicine and Health, University of Manchester, Manchester, United Kingdom; Department of Cardiology, Affiliated Hospital of Xuzhou Medical University, Xuzhou, China; The First Clinical Medical School, Xuzhou Medical University, Xuzhou, China; Jiangsu Key Laboratory of New Drug Research and Clinical Pharmacy, Xuzhou Medical University, Xuzhou, China.

|July 11, 2025

概括

巨细胞和介质蛋白-34 (IL-34) 通过促进类似节点的表型来增强鼻节 (SN) 功能. 然而,随着衰老而增加的miR-363-5p可能会逆转这些有益影响,影响心率调节.

科学领域:

心血管生物学心血管生物学
细胞和分子医学细胞和分子医学
再生医学是一种再生医学.

背景情况:

人类鼻节 (SN) 微环境涉及心脏纤维细胞和巨细胞,微RNA (miRNA) 和介质蛋白调节其功能.
这些因素影响心率的机制尚未完全理解.

研究的目的:

研究SN微环境的作用,包括miRNAs,interleukins,巨细胞和纤维细胞.
确定它们对诱导多能干细胞衍生的心肌细胞 (iPSC-CMs) 和心率调节的影响.

主要方法:

进行了多组学分析,比较人类的SN和右心房.
同培养的人类iPSC-CMs与M2型巨细胞 (M2s) 和纤维细胞.
在细胞和人血清样本中研究了介质素34 (IL-34) 信号通路和miRNA效应 (miR-363-5p).

主要成果:

在SN中确定了M2巨细胞和纤维细胞.
与M2s共同培养在iPSC-CMs中诱导了类似节点的表型,与M2s增加的IL-34分泌有关.
IL-34通过CSF1R/STAT3信号传递促进了这种表型,从而对HCN4.4进行上调. miR-363-5p抑制了M2分化并逆转了节点状转移;它在老年人中增加了IL-34,降低了SN功能障碍.

结论:

通过分泌IL-34,M2巨细胞有助于SN功能,通过HCN4上调增强SN活性.
与年龄相关的SN功能障碍中升高的miR-363-5p可能会抵消这些影响,可能会损害心率调节.

关键词:

心脏纤维细胞细胞.一个IL-34 - 一个IL-34.M2类型的巨细胞.阴道节的功能障碍鼻节微环境鼻节微环境在 iPSC-CMs 中使用.

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