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通过TLR9信号通路促进M1巨细胞极化,NET加速了大动脉的化

Luyao Liu^1,2, Zhenzhen Lan³, Xincan Liu⁴

¹Heart Center, The First Affiliated Hospital of Henan University of Chinese Medicine, Zhengzhou, 450000, Henan, China.

Molecular and cellular biochemistry

|August 26, 2025

概括

中性细胞细胞外陷 (NETs) 通过通过TLR9信号促进M1巨分化来驱动动动脉疾病 (CAVD). 抑制NET可能是延缓CAVD进展的治疗策略.

科学领域:

心血管生物学
免疫学
病理学

背景情况:

中性粒细胞外陷 (NETs) 参与了动脉疾病 (CAVD) 的发病.
连接NET与CAVD进展的确切机制尚不完全理解.

研究的目的:

阐明NET在CAVD病变中的作用.
研究NET对CAVD的巨分化和炎症反应的影响.
在CAVD小鼠模型中评估调节NET的治疗潜力.

主要方法:

使用促进化的饮食建立了CAVD小鼠模型.
使用Cl-amidine治疗进行调节的NET形成.
通过免疫光对素化素H3 (citH3) 的形成进行了评估.
使用ELISA,qRT-PCR和西式抹杀方法量化的炎症标志物 (TNF-α,IL-1β,IL-6),NET标志物 (MPO-DNA复合物) 和骨化因子 (BMP2,RUNX2).
在Raw264.7细胞上通过流细胞计分析了巨分离 (CD86,CD206).
在体外研究了TLR9信号的作用.

主要成果:

CAVD小鼠表现出明显的膜加厚,化,TNF-α,IL- 1β,MPO- DNA复合体,citH3,BMP2,RUNX2和TLR9的水平升高,IL-10的水平降低.
Cl- amidin治疗改善了CAVD表型,降低了炎症和NET标志物,并增加了IL-10.
在体外,CAVD血清诱导的NET通过TLR9信号促进M1巨分化,增加促炎细胞因子和降低IL-10.

结论:

通过TLR9信号通路促进M1巨分化,NETs有助于CAVD的进展.
在CAVD中,NET会加剧炎症反应.
针对NET是一种延缓CAVD进展的潜在治疗策略.

关键词:

动脉膜疾病巨细胞的两极分化中性粒细胞外陷

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