人类胚胎干细胞衍生的心血管祖细胞通过激活 PI3K/Akt 通路刺激心肌细胞的细胞周期活动。

IF 4.9 2区医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS

Journal of molecular and cellular cardiology Pub Date : 2024-10-10 DOI:10.1016/j.yjmcc.2024.10.002

Zhongyan Chen , Xiujian Yu , Minxia Ke , Hao Li , Yun Jiang , Peng Zhang , Jiliang Tan , Nan Cao , Huang-Tian Yang

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引用次数: 0

摘要

促进内源性心肌细胞增殖是修复梗死心脏的关键。植入人多能干细胞衍生的心血管祖细胞（hCVPCs）可促进梗死心脏的愈合。然而，人们对其对宿主心肌细胞增殖的影响知之甚少。在这里，我们发现将 hCVPC 植入小鼠梗死心脏可诱导宿主心肌细胞发生去分化和细胞周期再入，hCVPC 调节培养基在体外进一步证实了这一点。从机制上讲，PI3K/Akt 信号通路介导了 hCVPC 诱导的心肌细胞细胞周期重入。这些发现揭示了 hCVPC 在引发心肌细胞去分化和细胞周期活化方面的新功能，并强调了一种利用处于早期发育阶段的细胞使成年心肌细胞恢复活力的策略。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

Human embryonic stem cell-derived cardiovascular progenitor cells stimulate cardiomyocyte cell cycle activity via activating the PI3K/Akt pathway

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Human embryonic stem cell-derived cardiovascular progenitor cells stimulate cardiomyocyte cell cycle activity via activating the PI3K/Akt pathway

Promoting endogenous cardiomyocyte proliferation is crucial for repairing infarcted hearts. Implantation of human pluripotent stem cell-derived cardiovascular progenitor cells (hCVPCs) promotes healing of infarcted hearts. However, little is known regarding their impact on host cardiomyocyte proliferation. Here, we revealed that hCVPC implantation into mouse infarcted hearts induced dedifferentiation and cell cycle re-entry of host cardiomyocytes, which was further confirmed in vitro by hCVPC-conditioned medium. Mechanistically, the PI3K/Akt signaling pathway mediated hCVPC-induced cardiomyocyte cell cycle re-entry. The findings reveal the novel function of hCVPCs in triggering cardiomyocyte dedifferentiation and cell cycle activation and highlight a strategy utilizing cells at early developmental stages to rejuvenate adult cardiomyocytes.

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来源期刊

Journal of molecular and cellular cardiology 医学-细胞生物学

CiteScore

10.70

自引率

0.00%

发文量

171

审稿时长

42 days

期刊介绍： The Journal of Molecular and Cellular Cardiology publishes work advancing knowledge of the mechanisms responsible for both normal and diseased cardiovascular function. To this end papers are published in all relevant areas. These include (but are not limited to): structural biology; genetics; proteomics; morphology; stem cells; molecular biology; metabolism; biophysics; bioengineering; computational modeling and systems analysis; electrophysiology; pharmacology and physiology. Papers are encouraged with both basic and translational approaches. The journal is directed not only to basic scientists but also to clinical cardiologists who wish to follow the rapidly advancing frontiers of basic knowledge of the heart and circulation.