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通过依赖YTHDF1的PIEZO2 mRNA m6A修饰来对心脏纤维化进行表皮转录学调节

Ji-Fei Ding¹, Bin Tu¹, Kai Song¹

¹Department of Cardiothoracic Surgery, The Second Affiliated Hospital of Anhui Medical University, Hefei 230601, China.

Cardiovascular research

|November 5, 2024

概括

YTHDF1识别了Piezo2,通过m6A修饰控制心脏纤维细胞自和纤维化. 这一发现为预防心脏纤维化提供了新的策略.

科学领域:

心血管生物学心血管生物学
分子机制的分子机制
史诗转录组学史诗转录组学

背景情况:

机械敏感 (MS) 离子通道对于心脏功能和疾病至关重要.
皮埃佐家族MS通道在心脏纤维化中的作用在很大程度上仍未被探索.

研究的目的:

为了研究Piezo2在心脏纤维化中的作用.
为了阐明心脏纤维细胞中YTHDF1对Piezo2的表皮转录组调节.

主要方法:

在使用ISO/Ang-II/TAC模型的小鼠中诱导心脏纤维化.
利用AAV9传递用于YTHDF1和Piezo2.2的基因沉默.
进行RNA-seq,单细胞测序,组织学和生物化学分析.
在YTHDF1缺乏的心脏纤维细胞和小鼠心脏中研究了Piezo2的功能.

主要成果:

Piezo2表达,而不是Piezo1,在实验性心脏纤维化和TGF-β1诱导的心脏纤维细胞中增加.
纤维细胞特异性Piezo2缺乏减少纤维细胞激活,自和心脏纤维化.
YTHDF1与Piezo2mRNA结合,通过m6A修饰进行调节,增加了Piezo2翻译.
对Piezo2的EPITRANSCRIPTOMIC抑制改善了实验性心脏纤维化.

结论:

确定了一种涉及YTHDF1,m6A修饰和Piezo2的新型表皮转录学途径.
这种机制控制心脏纤维细胞自和纤维化.
这些发现表明,预防心脏纤维化是潜在的治疗点.

关键词:

这是一个Piezo22.自自是一种自的过程.心脏纤维化是什么心脏纤维化通过RNA甲基化.在 YTHDF1 的位置上.

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