通过ITE介导的AhR激活通过通过NF-κB/LCN2路径抑制促进巨细胞M2样极化来减轻动脉样硬化
Qiaowen Zheng1, Yifei Lin2, Lishan Zeng2
1Cardiovascular Department, Fuqing City Hospital, Fuzhou 350005, China.
Life sciences
|May 19, 2025
概括
使用ITE激活阿里碳水化合物受体 (AhR) 通过促进M2类巨细胞和抑制NF-κB/LCN2通路来减少动脉样硬化. 这表明AhR是AS的潜在治疗点.
科学领域:
- 心血管生物学 心血管生物学
- 免疫学 免疫学 免疫学
- 分子医学是分子医学.
背景情况:
- 动脉样硬化 (AS) 是一种由脂质积累和炎症驱动的慢性炎症性疾病.
- 巨细胞表型可塑性是AS病变发生的关键决定因素.
- 亚利碳化合物受体 (AhR) 参与调节巨细胞表型.
研究的目的:
- 调查 AhR 激活由其配体 ITE 在减弱 AS 的作用.
- 阐明 AhR 对巨细胞两极分化和AS 进展的影响的分子机制.
主要方法:
- 对于AhR,NF-κB和LCN2表达的西部涂抹.
- 流细胞计和免疫光学用于巨细胞的表型.
- 转录组测序以确定AhR调节的途径.
- 使用CUT&Tag-qPCR和lentivirus进行途径验证.
主要成果:
- ITE介导的AhR激活减少了动脉样硬化斑块面积和脂质沉积.
- 在体外和体内,ITE显著促进了M2类巨细胞的两极分化.
- 激活AhR抑制了NF-κB/LCN2信号通路,并将LCN2确定为关键目标.
- 抑制NF-κB/LCN2通路对于AhR驱动的M2极化至关重要.
结论:
- 激活AhR促进了类似M2的巨细胞两极分化,从而减弱了AS.
- 该机制涉及抑制NF-κB/LCN2通路.
- AhR是治疗动脉样硬化的有前途的治疗标.
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