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由miR-185-5p准的BASP1通过VSMC增殖和炎症促进动脉样硬化

Xinyun Xu¹, Shanyong Wu², Che Li³

¹Department of Emergency, The Second Affiliated Hospital of Jiaxing University Jiaxing 314000, Zhejiang, China.

American journal of translational research

|December 19, 2025

概括

大脑酸溶性蛋白1 (BASP1) 通过增加细胞增殖和亡来促进动脉样硬化. 针对miR-185-5p/BASP1通路可能为动脉样硬化提供新的治疗方法.

科学领域:

心血管生物学心血管生物学
分子医学是分子医学.

背景情况:

动脉样硬化 (AS) 是一种慢性炎症性疾病,其特点是动脉中积聚斑块.
大脑酸溶性蛋白1 (BASP1) 已涉及到各种细胞过程,但其在AS中的作用尚不清楚.

研究的目的:

阐明BASP1在动脉样硬化的发病过程中的功能作用和调节机制.
研究miR-185-5p/BASP1轴作为AS治疗点的潜力.

主要方法:

定量逆转录-聚合酶连锁反应 (qRT-PCR) 用于评估患者血清和细胞模型中的BASP1和miR-185-5p表达.
在实验室测试中使用人类动脉光滑肌细胞 (HUASMCs),用氧化低密度脂蛋白 (ox-LDL) 处理以模仿AS条件.
路西法酶记者基因测定证实了BASP1和miR-185-5p之间的直接向关系.

主要成果:

在AS患者的血清和ox-LDL治疗的HUASMC中,BASP1表达显著上调.
低调BASP1或上调miR-185-5p抑制了ox-LDL诱导的增殖,亡,炎症和粘附分子表达 (VCAM-1,ICAM-1).
miR-185-5p直接针对BASP1并对其进行负面调节;BASP1过度表达部分逆转了miR-185-5p模仿效应.

结论:

在HUASMCs中,BASP1促进了ox-LDL诱导的增殖和亡.
miR-185-5p/BASP1分子轴是AS预防和治疗的潜在治疗点.

关键词:

动脉样硬化是一种动脉样硬化.在BASP1中使用BASP.灭症 (apoptosis) 是一种死亡的过程.这是一种炎症炎症炎症炎症.在 miR-185-5p 中使用.

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