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辐射诱导的内皮铁死通过DDHD2-介导的Nrf2/GPX4通路加速动脉样硬化

Xi Su¹, Feng Liang², Ya Zeng¹

¹Department of Radiation Oncology, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200030, China.

|July 27, 2024

概括

辐射暴露加速动脉样硬化通过诱导内皮铁,一个涉及脂质过氧化过程. 含域蛋白2 (DDHD2) 通过Nrf2/GPX4通路来调节这种情况.

科学领域:

心血管生物学心血管生物学
辐射瘤学辐射瘤学
细胞机制细胞机制

背景情况:

辐射相关动脉样硬化 (RAA) 是一个严重的问题.
在RAA病变发生过程中,内皮铁的作用尚不清楚.

研究的目的:

调查RAA中内皮铁亡的参与.
阐明辐射诱导的内皮铁灭症背后的分子机制.

主要方法:

在活体RAA小鼠模型中接受了铁灭抑制剂的治疗.
使用暴露于辐射的人类动脉内皮细胞 (HAEC) 的体外研究.
蛋白质组学分析,基因淘汰和共同免疫沉试验.

主要成果:

RAA小鼠表现出增加的斑块负担和脂质过氧化,减少内皮细胞,由liproxstatin-1改善.
在HAECs中引起辐射的铁亡.
在HAEC中,DDHD2倒置导致脂质过氧化升高,GPX4和Nrf2表达降低.

结论:

辐射诱导的内皮铁亡加速了动脉样硬化.
通过Nrf2/GPX4通路,DDHD2是辐射诱导的内皮铁亡的潜在调节者.

关键词:

DDHD2 DDHD2 的意思是什么 Nrf2 / GPX4 在线播放脑内皮损伤的损伤铁性化 (ferroptosis) 是一种辐射相关动脉样硬化

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