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依赖SEC62的ER-phagy有助于阿佩林-13/APJ诱导的单细胞-血管内皮细胞粘附在动脉样硬化病原体中

Zhe Chen¹, Jun Cheng², Qun Zhou³

¹Institute of Pharmacy and Pharmacology, Hunan Province Cooperative Innovation Center for Molecular Target New Drug Study, College of Basic Medical Science, Hengyang Medical School, University of South China, Hengyang, China.

Acta pharmacologica Sinica

|February 10, 2025

概括

阿佩林-13触发了依赖SEC62的ER-phagy,促进单细胞粘附和动脉样硬化. 这个过程涉及UBL4A和ALDH1L1,为动脉样硬化提供潜在的治疗点.

科学领域:

心血管生物学心血管生物学
细胞自细胞自
动脉样硬化病原体的产生

背景情况:

单细胞对内皮细胞的粘附在动脉样硬化中至关重要.
ROS自途径与阿佩林-13诱导的单细胞内皮细胞粘附有关.

研究的目的:

为了研究apelin-13调节的特定类型的自.
阐明SEC62依赖ER-phagy在apelin-13诱导的单细胞内皮细胞粘附和动脉样硬化中的作用.

主要方法:

对阿佩林-13处理的HUVEC进行了转录组分析.
使用3MA和salubrinal的抑制研究.
在APOE-/-小鼠与SEC62删除的体内研究.
通过siRNA和突变分析调查UBL4A和ALDH1L1的参与.

主要成果:

阿佩林-13上调SEC62,诱导HUVEC中的ER-phagy,这种作用被抑制剂逆转.
在小鼠中,SEC62的删除减轻了动脉样硬化,减少了斑块面积和粘附分子.
阿佩林-13上调调节UBL4A,调解ALDH1L1的泛化,并促进依赖SEC62的ER-phagy.

结论:

阿佩林-13诱导了依赖SEC62的ER-phagy,促进单细胞-内皮细胞粘附和动脉样硬化.
在这个过程中,UBL4A-ALDH1L1通路是不可或缺的.
这项研究揭示了动脉样硬化的新机制,并确定了潜在的治疗点.

关键词:

这就是ALDH1L1的原因.阿佩林-13/APJ 在线播放这是ER-phagy.美国证券交易委员会62 SEC62 动脉样硬化动脉样硬化一个单细胞的粘附.

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