Developing cardiovascular systems use mechanical forces to take shape, but how ubiquitous blood flow forces instruct local cardiac cell identity is still unclear. By manipulating mechanical forces in vivo, we show here that shear stress is necessary and sufficient to promote valvulogenesis. We found that valve formation is associated with the activation of an extracellular adenosine triphosphate (ATP)–dependent purinergic receptor pathway, specifically triggering calcium ion (Ca²⁺) pulses and nuclear factor of activated T cells 1 (Nfatc1) activation. Thus, mechanical forces are converted into discrete bioelectric signals by an ATP-Ca²⁺-Nfatc1–mechanosensitive pathway to generate positional information and control valve formation.

中文翻译：

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生物电信号和对机械力响应的心脏细胞特性的控制

发展心血管系统使用机械力来形成，但无处不在的血流力如何指导局部心脏细胞身份仍不清楚。通过在体内操纵机械力，我们在此表明​​剪切应力对于促进瓣膜形成是必要且充分的。我们发现瓣膜形成与细胞外三磷酸腺苷 (ATP) 依赖性嘌呤能受体途径的激活有关，特别是触发钙离子 (Ca ²⁺ ) 脉冲和活化 T 细胞 1 (Nfatc1) 激活的核因子。因此，机械力通过 ATP-Ca ²⁺ -Nfatc1-机械敏感途径转换为离散的生物电信号，以产生位置信息和控制瓣膜的形成。