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宏细胞特异性UBA1淘汰通过通过BMAL1/CLOCK-REV-ERBα轴调节炎症反应来减轻败血症引起的肝功能障碍

Lu-Yuan Jin¹, Changting Cui¹, Si-Yi Lv¹

¹Department of Critical Care Medicine and Medical Research Center, Beijing Chao-Yang Hospital, Capital Medical University, No. 8 Worker's Stadium South Road, Beijing 100020, China.

International immunopharmacology

|November 8, 2025

概括

肝脏巨中的乌比基激活酶E1 (UBA1) 加剧了与败血症相关的肝功能障碍 (SALD). 抑制UBA1提高了生存率并减少了肝损伤,这表明UBA1是SALD的治疗点.

科学领域:

免疫学免疫学免疫学
肝病学肝病学是一种肝病学.
分子生物学分子生物学

背景情况:

巨细胞是败血症相关肝功能障碍 (SALD) 的关键参与者.
乌比基激活酶E1 (UBA1) 与蛋白质降解和炎症有关.
目前尚不清楚巨细胞UBA1在SALD病原体中的作用.

研究的目的:

研究巨UBA1在SALD的发展中的作用.
为了阐明底层的分子机制.
评估UBA1作为SALD的潜在治疗点.

主要方法:

已确定的败血症和急性肝损伤小鼠模型使用结和穿孔 (CLP).
生成的巨细胞特异性UBA1-Knockout (UBA1^M-KO) 和野生类型 (UBA1^M-WT) 的小鼠.
使用了体外共同培养系统和药理上抑制UBA1与PYR-41.1.

主要成果:

在CLP后,UBA1表达在肝脏组织和巨细胞中增加.
与UBA1^M-KO小鼠相比,UBA1^M-KO小鼠的生存率有所改善,肝功能障碍,炎症,氧化应激,脂质积累和肝细胞亡减少.
在实验室中,巨UBA1缺乏改善了LPS诱导的炎症反应和肝细胞损伤.
UBA1与BMAL1相互作用,促进其无化和降解,从而降低REV-ERBα活性并增加促炎性细胞因子的产生.
用PYR-41减弱的SALD进行选择性UBA1抑制.

结论:

巨细胞UBA1过度表达通过调节BMAL1-REV-ERBα轴来加剧SALD的病原性.
准UBA1为治疗SALD提供了一个有前途的治疗策略.

关键词:

在 BMAL1 中,肝脏功能障碍肝脏功能障碍这就是REV-ERBα.败血症这是一种败血症.在UBA1中,UBA1是UBA1的.

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