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纳米颗粒通过触发NCOA4-介导的ferritinophagy诱导HUVECs的铁化

Ziyuan Li¹, Yihua Wang², Jin Xu³

¹Department of Occupational Health and Environmental Health, School of Public Health, Qingdao University, Qingdao 266071, Shandong, People's Republic of China; Shandong Academy of Occupational Health and Occupational Medicine, Shandong First Medical University & Shandong Academy of Medical Sciences, Ji'nan 250062, Shandong, People's Republic of China.

Ecotoxicology and environmental safety

|December 27, 2023

概括

纳米颗粒 (SiNPs) 通过诱导人类静脉内皮细胞中的铁亡,可以引起心血管毒性. 这一过程涉及铁的积累,并由NCOA4依赖的铁代谢介导.

科学领域:

纳米技术纳米技术
心血管毒理学心血管毒理学
细胞生物学细胞生物学

背景情况:

纳米粒子 (SiNPs) 在包括生物医学在内的各种领域得到广泛应用.
对于人类暴露于SiNPs及其潜在的健康影响存在担忧.
SiNPs的心血管毒性及其潜在机制在很大程度上是未知的.

研究的目的:

研究SiNPs对人类静脉内皮细胞 (HUVEC) 的毒性影响.
阐明SiNP诱导的心血管毒性的机制,重点关注铁亡.

主要方法:

对HUVEC暴露于SiNPs的暴露.
评估细胞内铁含量和脂质过氧化.
线粒体形态分析.线粒体形态分析.
干预铁化剂脱胺甲基酸盐 (DFO) 和自抑制剂3-甲基氨酸 (3-MA).
核受体协活性剂4 (NCOA4) 的降解和费里丁重链1 (FTH1) 表达的评估.

主要成果:

在HUVEC中,SiNPs诱导铁,其特征是细胞内铁和脂质过氧化增加,并减少线粒体晶体.
DFO治疗缓解了SiNP诱导的铁亡.
自抑制部分降低了铁,表明它在这个过程中的作用.
NCOA4敲击抑制了FTH1,减少了细胞内铁和脂质过氧化,这表明NCOA4调解了SiNP诱导的铁亡.

结论:

在HUVEC中,SiNPs通过ferroptosis诱导心血管毒性.
在SiNP诱导的铁亡中,NCOA4介导的费里替诺法基起着重要作用.
这些发现为预防和治疗与SiNP暴露相关的心血管疾病提供了潜在的理论基础.

关键词:

自自是一种自的过程.心血管有毒性心血管毒性铁化是铁化的一种.没有NCOA4的纳米颗粒是一种.

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