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LncRNA MIR181A1HG 缺乏可以减轻血管炎症和动脉样硬化

Huaner Ni¹, Yulong Ge¹, Ying Zhuge¹

¹Department of Cardiology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, China (H.N., Y.G., Y.Z., X.L., H.C., J.L., W.L., X.W., G.S., Q.W., F.W.).

Circulation research

|March 6, 2025

概括

这项研究揭示了MIR181A1HG是动脉样硬化中血管炎症的关键驱动因素. 抑制MIR181A1HG可能为炎症性血管疾病提供新的治疗策略.

科学领域:

血管生物学和病理学
动脉样硬化的分子机制
长非编码RNA功能

背景情况:

内皮细胞 (EC) 功能障碍和血管炎症是动脉样硬化发展的核心因素.
长非编码RNAs (lncRNAs) 与血管病理有关,但它们在血管炎症中的特定作用需要进一步阐明.
MIR181A1HG,一个与miR-181a1/b1相邻的lncRNA,正在研究其在调节血管炎症方面的潜在作用.

研究的目的:

研究MIR181A1HG在调节血管炎症和动脉样硬化的作用.
阐明MIR181A1HG影响EC激活和炎症信号的分子机制.
评估针对MIR181A1HG在血管炎症疾病中的治疗潜力.

主要方法:

在人类和小鼠动脉样硬化病变中分析MIR181A1HG表达.
使用MIR181A1HG淘汰和过度表达模型进行功能丧失和功能获取研究.
通过RNA-蛋白相互作用试验,单细胞RNA测序和转录调节试验 (露西法酶报告员,ChIP) 调查分子机制.

主要成果:

在动脉样硬化病变中,MIR181A1HG表达升高,并促进NLRP3炎症酶激活,EC激活和病变形成.
缺少MIR181A1HG通过减少免疫细胞透和增强ECs中的抗炎途径来减少动脉样表型.
MIR181A1HG通过将Foxp1 (分叉盒转录因子1) 从目标基因促进体中隔离,独立于miR-181a1/b1,并由NF-κB (核因子kappa B) /p65.5调节.

结论:

MIR181A1HG通过Foxp1诱机制调节NLRP3炎症酶和EC激活,作为动脉样硬化中血管炎症的关键调节剂.
向MIR181A1HG为治疗血管炎症疾病提供了一个有希望的治疗途径.
这项研究强调了lncRNAs在动脉样硬化病变发生过程中的重要性.

关键词:

长非编码RNA,长非编码RNA.动脉样硬化动脉样硬化心血管疾病心血管疾病它们是内皮细胞的内皮细胞.炎症酶体 (inflammasomes) 是一种炎症酶体.

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