三甲基胺-N-氧化物影响小鼠大动脉中特定细胞类型的通路和网络,促进动脉样硬化斑块的脆弱性
Jenny Cheng1,2,3, Michael Cheng1,4, Satyesh Sinha3
1Department of Integrative Biology and Physiology (J.C., M.C., I.C., G.Z., I.S.A., G.D., X.Y.).
Arteriosclerosis, thrombosis, and vascular biology
|August 14, 2025
概括
三甲基胺-N-氧化物 (TMAO) 通过增加血管光滑肌细胞的亡和增强巨细胞介导的细胞外基质降解来促进斑块不稳定性,从而导致动脉样硬化中纤维状帽子变薄.
科学领域:
- 心血管生物学 心血管生物学
- 动脉样硬化研究 动脉样硬化研究
- 分子医学是分子医学.
背景情况:
- 三甲基胺-N-氧化物 (TMAO) 与动脉样硬化有关,但其直接的血管影响尚不清楚.
- 了解TMAO对血管细胞的影响对于了解动脉样硬化进展至关重要.
研究的目的:
- 研究TMAO在动脉样硬化中对血管细胞的细胞类型依赖和独立作用.
- 描述TMAO对基因表达和动脉样硬化倾向性血管系统的途径的影响.
主要方法:
- 在不同饮食 (控制,高胆固醇,高胆固醇+TMAO) 下对小鼠大动脉单细胞RNA测序.
- 细胞间通信和基因调控网络的分析.
- 在人类血管光滑肌细胞 (vSMCs) 中验证和小鼠斑块的组织学分析.
主要成果:
- 在vSMCs中,TMAO上调调的亡和下调的ECM组织/原基因.
- 巨细胞衍生的基因表达表明ECM降解是关键途径.
- TMAO减少了小鼠大动脉中的纤维盖厚度和原沉积.
结论:
- TMAO促进vSMC的亡,并减少ECM的形成.
- TMAO增强了巨细胞介导的ECM降解,增加了动脉样硬化斑块的不稳定性.
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