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巨细胞PIM1通过通过CD36增强泡细胞形成驱动动动脉硬化

Mirza Ahmar Beg^1,2, Quoc Quang Luu¹, Vaya Chen¹

¹Versiti Blood Research Institute, Milwaukee, WI, USA.

bioRxiv : the preprint server for biology

|November 24, 2025

概括

PIM1激酶调节巨细胞的CD36表达和脂质吸收,减少动脉样硬化. 针对这种PIM1/PPARγ/CD36通路,通过调节巨细胞脂质代谢,为治疗动脉样硬化提供了一种新的策略.

科学领域:

免疫学免疫学免疫学
细胞生物学细胞生物学
心血管研究研究心血管研究

背景情况:

动脉样硬化涉及巨细胞 (Mφ) 拾尸体受体CD36和脂肪斑块的积累.
在Mφ脂质处理和动脉生成中PIM1激酶的作用尚不清楚.
这项研究研究了PIM1在泡细胞形成和动脉样硬化期间对Mφs中CD36的调节.

研究的目的:

确定PIM1在调节巨细胞中CD36表达和功能的作用.
研究PIM1对巨细胞脂质处理和泡细胞形成的影响.
在体内评估Mφ特异性PIM1缺乏对动脉样硬化进展的影响.

主要方法:

在实验室研究中,使用PIM1缺乏和野生类型的小鼠巨细胞,用氧化LDL (oxLDL) 治疗.
在体内研究中,使用Mφ特异性PIM1缺乏和对照小鼠食高脂肪饮食.
对CD36,PIM1,oxLDL结合/吸收,泡细胞形成和动脉样硬化斑块大小的分析.

主要成果:

在Mφs中删除PIM1显著降低了CD36表达,oxLDL吸收和泡细胞形成.
缺少PIM1降低了PPARγ信号的调节,而PPARγ激动剂可以恢复这种信号.
在小鼠中,Mφ特异性PIM1缺乏明显减少了动脉样硬化斑块的形成.

结论:

通过PPARγ,PIM1是Mφs中CD36表达和活性的关键调节者.
PIM1-CD36通路促进Mφ脂质的积累和泡细胞的形成.
针对PIM1/PPARγ/CD36轴是一个潜在的动脉样硬化治疗策略.

关键词:

CD36 CD36 CD36 CD36 CD36 CD36 CD36 CD36 CD36 CD36 CD36 CD36 CD36 CD36 在PIM1中,PIM1是PIM1.在 PPARγγ 中.动脉样硬化动脉样硬化脂质脂质是什么意思脂质脂质是什么意思巨细胞是什么?巨细胞是什么?

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