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长非编码RNANAV2-AS2通过通过与NAV2mRNA的感觉-反感觉杂交形成来调节EndMT,从而防止动脉样硬化

Guoqing Liu¹, Lin Zhu¹, Huiying Cai¹

¹School of Pharmacy, Shandong University of Traditional Chinese Medicine, Jinan 250000, Shandong, China; School of Pharmacy, Jining Medical University, Rizhao 276800, Shandong, China.

International journal of biological macromolecules

|July 18, 2025

概括

长非编码RNANAV2-AS2通过防止内皮细胞转化为介质细胞转化 (EndMT) 来抑制动脉样硬化. 过度表达NAV2-AS2减少了小鼠的动脉样硬化,突出了其对心血管疾病的治疗潜力.

科学领域:

心血管生物学心血管生物学
分子医学是分子医学.
在RNA生物学,RNA生物学.

背景情况:

动脉样硬化是心血管疾病的主要原因之一.
长非编码RNAs (lncRNAs) 与动脉样硬化病变发生有关.
内皮转介质转换 (EndMT) 有助于动脉样硬化斑块的发展.

研究的目的:

为了识别涉及动脉样硬化的新 lncRNAs.
研究 lncRNA NAV2-AS2 在动脉样硬化和EndMT中的作用.
阐明NAV2-AS2在调节EndMT中的分子机制.

主要方法:

微阵列分析以确定与动脉样硬化相关的 lncRNAs.
在人血清,小鼠模型和细胞培养中进行表达分析.
在活体研究中,在ApoE-/-小鼠中使用腺相关病毒 (AAV) 介导的基因传递.
涉及RNA双重形成的机制研究,mRNA稳定性测试和蛋白质-蛋白质相互作用分析.

主要成果:

在动脉样硬化患者,小鼠模型和牛-LDL刺激细胞中,NAV2-AS2表达减少.
在内皮细胞中NAV2-AS2的过度表达在ApoE-/-小鼠中预防和治疗了饮食诱导的动脉样硬化.
NAV2-AS2通过与NAV2mRNA形成双重体来抑制EndMT,使其稳定,并增加NAV2蛋白水平.
NAV2-AS2增强了NAV2与牛的相互作用,导致牛蛋白降低调节和抑制EndMT.

结论:

NAV2-AS2作为EndMT的新型抑制剂,并具有抗动脉样硬化性质.
NAV2-AS2/NAV2/Snail轴是调节动脉样硬化中的EndMT的关键通路.
NAV2-AS2代表了动脉样硬化和相关心血管疾病的潜在治疗标.

关键词:

动脉样硬化是一种动脉样硬化.最终的MT 结束的MT 的NAV2 的NAV2 在NAV2-AS2中,可以选择NAV2-AS2.一个牛牛牛.

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