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HNF4A通过抑制NCOA4介导的费里替诺来改善急性肝衰竭

Weiyan Yu¹, Caiyan Zhao²

¹Department of Infectious Diseases, The Third Hospital of Hebei Medical University, Shijiazhuang, 050000, China.

Scientific reports

|August 13, 2025

概括

核受体协活性剂4 (NCOA4) 在急性肝衰竭 (ALF) 中被上调,促进铁亡. 抑制NCOA4可以缓解肝损伤,而HNF4A-NCOA4轴为ALF提供了潜在的治疗点.

科学领域:

细胞生物学细胞生物学
肝病学肝病学是一种肝病学.
疾病的分子机制.

背景情况:

不平衡的细胞内铁平衡有助于铁和炎症性疾病.
通过NCOA4介导的费里自调节铁,但其在急性肝衰竭 (ALF) 中的作用尚不清楚.

研究的目的:

研究NCOA4在肝细胞铁亡和ALF进展中的作用和调节机制.
在ALF病变发生过程中探索HNF4A-NCOA4轴.

主要方法:

在人类肝脏组织和ALF/对照小鼠模型中对NCOA4蛋白表达的比较分析.
在体外和体内实验涉及基因沉默和炎症刺激 (LPS) 的实验.
评估铁灭菌标记物,线粒体形态学和基因表达调节.

主要成果:

在患有HBV-ACLF,ALF模型小鼠和炎症性肝细胞的患者中,NCOA4表达显著升高.
沉默NCOA4可以减轻肝细胞中LPS诱导的铁亡.
肝核因子4A (HNF4A) 通过转录抑制NCOA4,通过抗费里丁自降低铁亡.

结论:

HNF4A-NCOA4轴在肝细胞铁和ALF病变发生过程中发挥着关键作用.
准HNF4A-NCOA4轴为急性肝衰竭提供了一个潜在的治疗策略.

关键词:

严重的肝衰竭是急性肝衰竭.铁性化 (ferroptosis) 是一种肝细胞肝细胞肝细胞核因子4A 肝细胞核因子4A 核受体协活性剂 4 核受体协活性剂

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