肝细胞癌
索拉非尼
GPX4
程序性细胞死亡
脂质过氧化
过氧化脂质
细胞
医学
生物
癌症研究
细胞凋亡
氧化应激
内科学
遗传学
谷胱甘肽过氧化物酶
过氧化氢酶
作者
Yulang Jiang,Yongxin Yu,Zhengying Pan,Christian Glandorff,Mingyu Sun
标识
DOI:10.1038/s41420-024-01863-1
摘要
Abstract Ferroptosis is an iron ion-dependent, regulatory cell death modality driven by intracellular lipid peroxidation that plays a key role in the development of HCC. Studies have shown that various clinical agents (e.g., sorafenib) have ferroptosis inducer-like effects and can exert therapeutic effects by modulating different key factors in the ferroptosis pathway. This implies that targeting tumor cell ferroptosis may be a very promising strategy for tumor therapy. In this paper, we summarize the prerequisites and defense systems for the occurrence of ferroptosis and the regulatory targets of drug-mediated ferroptosis action in HCC, the differences and connections between ferroptosis and other programmed cell deaths. We aim to summarize the theoretical basis, classical inducers of ferroptosis and research progress of ferroptosis in HCC cells, clued to the treatment of HCC by regulating ferroptosis network. Further investigation of the specific mechanisms of ferroptosis and the development of hepatocellular carcinoma and interventions at different stages of hepatocellular carcinoma will help us to deepen our understanding of hepatocellular carcinoma, with a view to providing new and more precise preventive as well as therapeutic measures for patients.
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