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METTL14 通过m6A甲基化 TEAD1 mRNA促进血管光滑肌肉细胞的增殖和Neointima形成

Liang Wang^1,2, Guojin Xia^1,2, Yan Tang^1,2

¹Department of Cardiology, The First Affiliated Hospital of Nanchang University, Nanchang, China.

Journal of biochemical and molecular toxicology

|May 13, 2025

概括

甲基转移酶样14 (METTL14) 通过稳定TEAD1 mRNA,促进血管光滑肌肉细胞的增殖和血管重塑. 这一发现为诸如动脉样硬化等心血管疾病提供了新的治疗点.

科学领域:

心血管生物学心血管生物学
表观遗传学在表观遗传学中,表观遗传学是指表观遗传学.
分子医学是分子医学.

背景情况:

血管光滑肌细胞 (VSMC) 增殖和新极性增生是动脉样硬化和血管形成术后复原症的关键驱动因素.
之前的研究确定了TEA域转录因子1 (TEAD1) 作为VSMC差异化的调节者.

研究的目的:

研究甲基转移酶样14 (METTL14) 在血管改造中的作用.
阐明METTL14影响VSMC行为和血管病理的分子机制.

主要方法:

在人类动脉样硬化斑块和小鼠动脉损伤模型中分析METTL14表达.
使用人类冠状动脉光滑肌细胞 (HCASMCs) 进行体外研究,以评估METTL14过度表达和淘汰的影响.
在体内研究涉及小鼠的导线诱导的动脉损伤.
研究TEAD1mRNA的m6A修饰及其对YAP1/TEAD1信号传递的影响.

主要成果:

在动脉样硬化动脉中,METTL14表达被上调,与VSMC脱差相关.
过度表达METTL14促进了VSMC的扩散和迁移,而敲击减轻了新极限增生症.
发现METTL14通过核酸513的m6A修饰稳定了TEAD1mRNA,从而增强了YAP1/TEAD1信号传递.
抑制METTL14介导的信号传递恢复了VSMC的分化和抑制了增殖.

结论:

通过METTL14介导的TEAD1mRNA的m6A修饰是一种新的驱动血管病理的机制.
针对METTL14-TEAD1轴为心血管疾病提供了潜在的治疗策略.

关键词:

在METTL14中,使用的是METTL14 N6 - - 甲基氨胺.我们的 TEAD1 团队.新亲密的形成形成.它们的扩散和扩散.

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