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在动脉样硬化发展中,FUS/Sfrp5/Wnt5的表达和影响

Xiaogao Wang¹, Hui Wang², Ran Lu¹

¹Department of Vascular Surgery, The First Affiliated Hospital of Bengbu Medical University, Bengbu, Anhui, China.

Annals of clinical and laboratory science

|May 9, 2025

概括

FUS和Sfrp5协同抑制Wnt5a的表达,为动脉样硬化 (AS) 提供一种潜在的治疗策略. 这项研究揭示了它们对控制AS进展的综合作用.

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.
细胞病理学细胞病理学

背景情况:

动脉样硬化 (AS) 是导致心血管疾病的主要原因之一,患者的治疗结果不令人满意.
目前对AS的医疗治疗需要加强,以改善患者的预后.

研究的目的:

研究FUS和Sfrp5在动脉样硬化中的FUS/Sfrp5/Wnt5a通路中的作用.
探索改善AS治疗结果的潜在治疗目标.

主要方法:

在人类血管光滑肌细胞 (HVSMCs) 中使用氧化低密度脂蛋白 (OX-LDL) 建立了AS细胞模型.
采用了包括Western blot,Transwell测定,CCK8测定,Oil Red O染色和ELISA在内的技术来分析FUS/Sfrp5/Wnt5a通路.
根据AS模型进行了oe-NC,oe-FUS,oe-Sfrp5或oe-FUS+oe-Sfrp5的管理.

主要成果:

在AS模型中发现FUS和Sfrp5都抑制了Wnt5a的表达.
在OX-LDL诱导的HVSMC中,FUS对脂质滴形成和迁移表现出抑制作用.
在控制Wnt5a表达方面观察到FUS和Sfrp5之间的协同效应.

结论:

在动脉样硬化背景下,FUS和Sfrp5在调节Wnt5a方面表现出协同作用.
准FUS和Sfrp5通路为控制AS进展提供了一个有希望的治疗途径.

关键词:

在FUS/Sfrp5/Wnt5中使用.动脉样硬化动脉样硬化有协同效应的效应.

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