核因子κB信号通路调控铁死亡的机制及在肝脏疾病中的作用

程新月; 史文杰; 刘熔; 禄保平

doi:10.12449/JCH250835

核因子κB信号通路调控铁死亡的机制及在肝脏疾病中的作用

DOI: 10.12449/JCH250835

程新月¹,
史文杰¹,
刘熔¹,
禄保平^{1, 2, , ,}

1.
河南中医药大学第二临床医学院，郑州 450046
2.
河南中医药大学肝病研究所，郑州 450046

基金项目:

河南省中医药科学研究专项课题 (2022ZY1167);

河南省中医药科学研究专项课题 (2024ZY2156);

全国名中医传承工作室建设项目 (National Chinese Medicine Office Human Education Letter ［2018］ No.119)

利益冲突声明：本文不存在任何利益冲突。

作者贡献声明：程新月负责撰写论文及绘制图片；史文杰负责课题设计及修改论文；刘熔负责文献检索及整理；禄保平负责拟定写作思路及最后定稿。

详细信息

通信作者:
禄保平， lbp1921@sohu.com （ORCID： 0000-0002-3707-2185）

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出版历程
- 收稿日期: 2024-11-25
- 录用日期: 2025-01-07
- 出版日期: 2025-08-25

Mechanism of the nuclear factor-kappa B signaling pathway regulating ferroptosis and its role in liver diseases

Xinyue CHENG¹,
Wenjie SHI¹,
Rong LIU¹,
Baoping LU^{1, 2
, ,
,}

1.
The Second Clinical Medical College Henan University of Chinese Medicine，Zhengzhou 450046，China
2.
Institute of Hepatology Henan University of Chinese Medicine，Zhengzhou 450046，China

Research funding:

The Special Research Project of Traditional Chinese Medicine in Henan Province (2022ZY1167);

The Special Research Project of Traditional Chinese Medicine in Henan Province (2024ZY2156);

National Famous Traditional Chinese Medicine Practitioner Inheritance Workshop Construction Project (National Chinese Medicine Office Human Education Letter ［2018］ No.119)

More Information

Corresponding author: LU Baoping， lbp1921@sohu.com （ORCID： 0000-0002-3707-2185）

摘要

摘要: 核因子κB（NF-κB）信号通路作为一种经典的炎症反应通路，在多种生理和病理过程中发挥着关键作用。铁死亡是一种新的非凋亡性细胞死亡形式，研究发现NF-κB信号通路与铁死亡之间存在紧密联系，影响着肝脏系统疾病的发生发展过程。因此，靶向NF-κB信号通路调节铁死亡在肝脏系统疾病的治疗中有巨大潜力。本文探讨了NF-κB信号通路对铁死亡过程中脂质代谢、铁离子代谢等关键环节的影响，以及正向或负向调控铁死亡的作用机制。同时，探讨了该信号通路调控铁死亡在肝损伤、非酒精性脂肪性肝病、酒精性肝病和肝细胞癌等肝脏系统疾病中的研究进展，为进一步理解肝脏疾病的发病机制以及开发新的治疗策略提供参考。
- 核因子-κB /
- 铁死亡 /
- 肝疾病
Abstract: As a classical inflammatory response pathway， the nuclear factor-kappa B （NF-κB） signaling pathway plays a critical role in various physiological and pathological processes. Ferroptosis is a new form of non-apoptotic cell death， and recent studies have shown that there is a strong link between the NF-κB signaling pathway and ferroptosis， which affects the development and progression of liver diseases. Therefore， regulation of ferroptosis by targeting the NF-κB signaling pathway has a great potential in the treatment of liver diseases. This article discusses the influence of the NF-κB signaling pathway on the critical links such as lipid metabolism and iron metabolism during ferroptosis， as well as its mechanism of action in the positive and negative regulation of ferroptosis. Meanwhile， this article reviews the research advances in the role of this signaling pathway in liver diseases such as liver injury， nonalcoholic fatty liver disease， alcoholic liver disease， and hepatocellular carcinoma through the regulation of ferroptosis， so as to provide a reference for further understanding of the pathogenesis of liver diseases and the development of new therapeutic strategies.
- Nuclear Factor-κB /
- Ferroptosis /
- Liver Diseases

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注： NQO1，NADPH醌氧化还原酶1；MDA，丙二醛；Fe²⁺，二价铁离子；FPNI，铁转运蛋白1；FTH1，铁蛋白重链1。

图 1 NF-κB信号通路在铁死亡中的作用

Figure 1. The role of the NF-κB signaling pathway in ferroptosis

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表 1 肝疾病中基于NF-κB信号通路的铁死亡调控分子及调控机制

Table 1. Regulatory molecules and mechanisms of ferroptosis based on NF-κB signalling pathway in liver diseases

疾病类型	第一作者及年份	药物靶点	作用机制	NF-κB 表达	作用影响	作用结果
肝损伤	Chen^［43］2022	组蛋白H3	NOD2/IκBα/ NF-κB p65	激活	Fe²⁺、ROS↑ GPX4、GSH↓	诱导急性肝衰竭肝巨噬细胞铁死亡
肝损伤	Zhong^［44］2021	NF-κB诱导激酶NIK	NIK/IKKα/ROS	激活	ROS↑	促进肝细胞铁死亡，加重肝损伤
肝损伤	Tak^［46］2024	NEMO	NEMO/Gα12/ GPX4	抑制	GPX4↑	保护肝细胞免受内质网应激诱导的铁死亡
肝损伤	Lin^［47］2023	Caspase 6	NEMO/RIPK1/ IκBα	激活	ASCL4↑GPX4↓	促进肝细胞铁死亡
MAFLD	Yao^［50］2024	牙龈卟啉单胞菌	NF-κB/GPX4/ SLC7A11	激活	GPX4、SLC7A11↓	诱导MAFLD细胞铁死亡
MAFLD	Yu^［51］2021	EWCD	Nrf2/NF-κB/ROS	抑制	ROS↓	抑制MAFLD细胞铁死亡
MAFLD	Yuan^［52］2023	HMOX1	NF-κB/SLC7A11/ GPX4	抑制	SLC7A11、GPX4↑	抑制铁死亡，缓解非酒精性脂肪性肝炎
ALD	Zmijewski^［55］ 2014	酒精	HAMP mRNA/ NF-κB/Fe²⁺	激活	Fe²⁺↑	促进酒精性肝病细胞铁死亡
HCC	Yao^［57］2021	LIFR	LIFR/NF-κB/ LCN2	激活	Fe²⁺↓	减弱HCC对铁死亡的敏感性
HCC	Sun^［58］2024	Bay11-7082	NF-κB/GPX4/ ROS	抑制	ROS、MDA、Fe²⁺↑	促进HepG2细胞铁死亡
HCC	Wang^［59］2023	阿司匹林	NF-κB/SLC7A11	抑制	SLC7A11↓	促进HCC细胞铁死亡
HCC	Lin^［60］2023	白术内酯Ⅱ	TRAF6/NF-κB/ ROS	抑制	ROS、MDA↑，GSH、 SLC7A11、GPX4↓	促进HCC细胞铁死亡
HCC	Li^［61］2024	DDX5	Wnt/β-catenin/ NIK/p52/RelB	激活	Nrf2↑	抑制索拉非尼诱导的HCC细胞铁死亡
注：Gα12，G蛋白亚基α12；Bay11-7082，NF-κB抑制剂；↑，上升或激活；↓，下降或抑制。

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