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巨细胞中的NHE1通过依赖的ROS和NLRP3炎症酶激活促进了八性/Olfr2诱导的动脉样硬化

Tianhui Wang^1,2, Lan Wang^1,2, Qian Tian^1,2

¹School of Clinical medicine, Guizhou Medical University, Guiyang, 550025, China.

Scientific reports

|December 29, 2025

概括

通过增加斑块中的-交换器1 (NHE1) 来加剧动脉样硬化. 针对嗅觉受体2 (Olfr2) 的下游效应因子NHE1,为动脉样硬化提供了一个潜在的治疗策略.

科学领域:

心血管研究研究心血管研究
分子生物学分子生物学
免疫学免疫学免疫学

背景情况:

动脉样硬化 (AS) 是一个主要的全球健康问题.
在AS巨细胞中,-交换器1 (NHE1) 和嗅觉受体2 (Olfr2) 的作用尚不清楚.
了解这些相互作用对于开发新疗法至关重要.

研究的目的:

为了研究八甲醇对AS发育和NHE1表达的影响.
阐明AS中八性,Olfr2和NHE1之间的分子机制.
评估NHE1作为AS的潜在治疗点.

主要方法:

使用ApoE-/-小鼠和RAW264.7巨细胞进行体内和体外研究.
服用八醇和NHE1抑制剂,评估AS进展,炎症和泡细胞的形成.
采用RNA干扰和化来探索潜在的信号通路.

主要成果:

在体内通过调节斑块NHE1而加剧了Octanal AS;NHE1缺乏减少了AS和炎症.
在体外,八性剂量和时间依赖性增加了RAW264.7细胞NHE1的表达和活性,促进泡细胞的形成.
抑制NHE1减弱了八内诱导的效应;Olfr2向或合降低了NHE1上调和炎症.

结论:

通过AS中的Olfr2通路,NHE1通过八性上调.
NHE1 作为一个关键的下游调解者,在八性诱导的AS进展.
准NHE1为治疗动脉样硬化症提供了一个有前途的治疗策略.

关键词:

动脉样硬化是一种动脉样硬化.炎症炎症是一种炎症.八式的八式的嗅觉受体 2 嗅觉受体 2 嗅觉受体交换器 1 交换器 1

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