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NAT10通过mRNA ac4C乙化促进血管重塑

Cheng Yu^1,2,3,4, Yue Chen^2,3,4, Hao Luo^2,3,4

¹Department of Cardiology, Fujian Medical Center for Cardiovascular Diseases, Fujian Institute of Coronary Heart Disease, Fujian Medical University Union Hospital, Fuzhou, P.R. China.

European heart journal

|October 25, 2024

概括

N-乙转移酶10 (NAT10) 通过乙化信使RNA (mRNA) 来促进血管重塑. 使用雷莫德林抑制NAT10可降低新密细胞的形成和血管光滑肌细胞 (VSMC) 的增殖,为心血管疾病提供潜在的治疗策略.

科学领域:

分子生物学分子生物学
心血管研究研究心血管研究
表观遗传学在表观遗传学中,表观遗传学是指表观遗传学.

背景情况:

血管光滑肌细胞 (VSMC) 现型切换是心血管疾病的关键因素.
由N-乙转移酶10 (NAT10) 催化的RNA的N4-乙基提丁 (ac4C) 修饰在生理和病理过程中起作用.
在血管疾病中mRNA ac4C修饰的特定功能尚不清楚.

研究的目的:

研究NAT10和mRNAac4C修饰在血管疾病中的作用.
阐明NAT10影响血管重塑的潜在机制.
评估针对NAT10在血管疾病中的治疗潜力.

主要方法:

使用了体外和体外血管损伤模型.
使用RNA测序 (RNA-seq),乙化mRNA免疫沉降测序 (acRIP-seq) 和RNA结合蛋白免疫沉降测序 (RIP-seq) 来识别机制.
使用雷莫德林评估了NAT10抑制的效果.

主要成果:

在受伤的动脉中,NAT10和ac4C的修饰升高.
在VSMC中NAT10删除减少了neointima形成和VSMC表型切换.
NAT10直接针对ITGB1和Col1a2等mRNA,增加ITGB1mRNA的稳定性和FAK信号传递,促进VSMC的增殖和血管重塑.
雷莫德林的使用通过抑制VSMC增殖和FAK信号,抑制了neointima的形成.

结论:

NAT10通过mRNA ac4C乙化促进血管重塑.
准NAT10是一种有前途的治疗策略,可以预防血管重塑.
NAT10-ac4C-ITGB1通路是VSMC表型和血管疾病进展的关键调节者.

关键词:

表观遗传学在表观遗传学中,表观遗传学是指表观遗传学.在 NAT10 中,NAT10 包含了NAT10.血管改造是指进行血管改造.血管光滑肌细胞是血管光滑肌细胞 mRNA是N4-乙基胺的一种.

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