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菲西通过调节HNRNPA1-介导的铁死来改善血管化

Qiang Feng¹, Lan He², Yang He³

¹Division of Cardiology, The First Affiliated Hospital of Soochow University, Suzhou, China; Division of Cardiology, Handan Central Hospital, Handan, China.

Annals of vascular surgery

|June 24, 2025

概括

发现天然化合物菲塞通过抑制细胞死亡的一种类型 - - 铁死来减少血管化. 在细胞和动物模型中,这种效应是由HNRNPA1蛋白调节的介导.

科学领域:

生物化学生物化学
细胞生物学细胞生物学
药理学药理学是指药理学的学科.

背景情况:

菲塞具有抗炎,抗氧化和抗瘤的特性.
菲塞丁可以抑制与铁死相关的氧化应激,可能减轻动脉样硬化进展.

研究的目的:

为了研究菲塞丁对血管化的作用.
为了探索fisetin和ferroptosis在血管化中的相互作用.

主要方法:

使用高酸盐诱导的大动脉光滑肌细胞 (ASMC) 和用维生素D3/尼古丁治疗的老鼠建立了血管化模型.
在ASMC中,使用不同度的菲塞,费罗斯塔-1 (ferroptosis抑制剂),埃拉斯 (ferroptosis诱导剂) 和HNRNPA1 siRNA进行了治疗.
大鼠每天服用菲塞.

主要成果:

费塞丁剂量取决于HP治疗的ASMC中改善了化和降低了铁亡标志物.
费罗斯塔丁-1 减少了化,而埃拉斯则加剧了化,部分扭转了菲塞的作用.
菲塞丁上调调节了HNRNPA1;HNRNPA1 siRNA减弱了菲塞丁对化和铁亡的保护作用.
在老鼠中,菲塞降低了血管化,调节了化和与铁死相关的基因表达.

结论:

菲西通过调节HNRNPA1介导的铁死来改善血管化.
这些发现在细胞和动物模型中一致,表明临床前的治疗潜力.

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