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F-53B通过ferroptosis相关途径刺激了血管光滑肌细胞表型切换和血管重塑

Min Zhang¹, Jun Shi², Huichao Pan¹

¹Institute of Cardiovascular Diseases, Division of Cardiology, Tongren Hospital, Shanghai Jiao Tong University School of Medicine, 200336, China.

The Science of the total environment

|September 28, 2024

概括

6:2化多化乙太硫酸盐 (F53B) 暴露会导致血管光滑肌肉细胞铁亡和重塑. 一种铁化剂逆转了这些效应,揭示了F53BB.

科学领域:

环境毒理学环境毒理学
心血管研究的心血管研究.
细胞毒理学细胞毒理学

背景情况:

6:2化多乙烯硫酸盐 (F53B) 是一种在中国广泛使用的PFOS替代品.
虽然F53B的毒性已知,但其在血管重塑中的作用尚不清楚.

研究的目的:

研究F53B对血管光滑肌肉细胞 (VSMC) 功能的影响.
阐明F53B促进血管重塑的机制.

主要方法:

血管形态的体内研究.
表型和分子测定以评估VSMC铁和表型切换.
铁素-1 (Fer-1) 治疗可以逆转F53B的影响.
对与铁亡相关的途径的分析 (ATR,LOC101929922/miR-542-3p/ACSL4).

主要成果:

在体内,F53B诱导了血管形态变化.
暴露于F53B导致了过度的VSMC铁和表型切换.
铁-1治疗改善了F53B诱导的VSMC功能障碍和血管重塑.
F53B激活了ATR和LOC101929922/miR-542-3p/ACSL4铁灭菌通路. 这种激活的原因是:F53B激活了ATR和LOC101929922/miR-542-3p/ACSL4铁灭菌通路.

结论:

通过VSMC铁和表型切换,F53B诱导了血管重塑.
该ATR和LOC101929922/miR-542-3p/ACSL4通路与F53B的血管毒性有关.
需要进一步评估F53B的血管毒性风险.

关键词:

这是一个ATRATRATRATR.美国F-53B战斗机铁性化 (ferroptosis) 是一种 LOC101929922/miR-542-3p/ACSL4 在美国血管改造是指进行血管改造.血管光滑肌肉细胞表型开关血管光滑肌肉细胞表型开关

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