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扰乱的剪切应力通过TRIM21调节的MAPK6降解和由此产生的内皮炎症促进动脉样硬化

Feng Wang¹, Shu-Yu Wang¹, Yue Gu¹

¹Division of Cardiology, Nanjing First Hospital, Nanjing Medical University, Nanjing, China.

Clinical and translational medicine

|January 7, 2025

概括

扰乱的剪切应力减少了内皮细胞中的MAPK6蛋白,促进了斑块的形成. 通过减少炎症,保护MAPK6提供了针对动脉样硬化的新疗法策略.

科学领域:

心血管生物学心血管生物学
动脉样硬化的分子机制
内皮细胞生物学内皮细胞生物学

背景情况:

冠状动脉斑块的形成与扰乱的剪切应力 (DSS) 有关.
在DSS下驱动斑块发展的机制尚未完全理解.
在剪切应激诱导的血管变化中MAPK6的作用需要阐明.

研究的目的:

为了研究MAPK6在对干扰剪切应力的内皮反应中的作用.
确定MAPK6对动脉样硬化发展和进展的影响.
为了确定由MAPK6在内皮炎症中调节的分子通路.

主要方法:

在体外和体外模型,包括ApoE-/-小鼠和AAV-MAPK6输送.
RNA测序 (RNA-seq) 和单细胞RNA-seq用于全面的基因表达分析.
同免疫沉 (CO-IP),蛋白质组分析和条件淘汰的小鼠模型 (ApoE-/-MAPK6flox/floxTEKCre).

主要成果:

干扰剪切应力 (DSS) 通过TRIM21介导的无处置和降解降低了内皮MAPK6蛋白水平.
在内皮细胞中MAPK6的过度表达在ApoE-/-小鼠中显示出抗动脉样硬化作用.
MAPK6通过EGR1/CXCL12信号轴调节内皮炎症.
在内皮细胞中MAPK6的有条件淘汰会加剧炎症和斑块生长,通过CXCL12中和可逆效应.

结论:

通过减轻内皮炎症,MAPK6对动脉样硬化起着保护作用.
干扰的流动触发了MAPK6的降解,导致斑块的进展.
向MAPK6或EGR1/CXCL12轴为动脉样硬化提供了潜在的治疗途径.

关键词:

在MAPK6中,您可以使用MAPK6.在 TRIM2121 中.动脉样硬化动脉样硬化内皮内皮炎的炎症剪切压力的压力.

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