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NRF1协调线粒体适应以抑制细胞内ROS和炎症反应在缺血再输液期间

Jiakun Li^1,2, Jiawei Yan³, Guowei Tu⁴

¹Department of Anesthesiology, Zhongshan Hospital, Fudan University, Shanghai, China.

Cell death discovery

|May 15, 2025

概括

在巨细胞中,核因子红色素2像1 (NRF1) 通过控制线粒体功能和减少氧化应激,减轻缺血再流损伤 (IRI). 缺少它会在IRI期间加剧损伤和炎症.

科学领域:

免疫学免疫学免疫学
细胞生物学细胞生物学
生理学生理学生理学

背景情况:

缺血重灌损伤 (IRI) 涉及氧化应激和炎症,其中巨细胞起着关键作用.
活性氧物种 (ROS) 在IRI中影响巨细胞反应的确切机制尚未完全理解.

研究的目的:

研究ROS和巨适应在IRI中的作用.
在IRI中确定线粒体平衡和炎症反应的关键调节者.

主要方法:

在重氧化过程中分析巨细胞线粒体动力学 (裂变,融合) 和全方位蛋白酶体系统 (UPS) 流量.
调查转录因子核因子红色素2像1 (NRF1) 响应ROS的诱导和功能.
使用IRI的小鼠模型来评估骨髓NRF1缺乏对损伤和炎症的影响.

主要成果:

在IRI中,巨体在重氧化过程中表现出线粒体裂变和增加的UPS流量.
ROS迅速诱导NRF1,它可以调节UPS和线粒细胞分裂通路,促进线粒体融合/裂变动态,并减少ROS.
在IRI模型中,小鼠缺少髓状NRF1会导致ROS升高,炎症加剧,损伤恶化.

结论:

巨细胞NRF1在IRI期间是线粒体平衡和抗氧化剂防御的关键调节者.
在巨细胞中激活NRF1可减轻氧化应激,减轻炎症反应,从而防止IRI.
向巨细胞NRF1可能为缓解IRI和相关器官损伤提供治疗策略.

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