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铁死亡在各种慢性肝病中的新兴作用:机遇还是挑战

The Emerging Role of Ferroptosis in Various Chronic Liver Diseases: Opportunity or Challenge.

作者信息

Zhu Lujian, Luo Shengnan, Zhu Yin, Tang Shiyue, Li Chenge, Jin Xiaozhi, Wu Faling, Jiang Huimian, Wu Lina, Xu Yejin

机构信息

Department of Infectious Diseases, Jinhua Municipal Central Hospital, Jinhua, People's Republic of China.

Department of Infectious Diseases, Taizhou Enze Medical Center (Group), Enze Hospital, Taizhou, People's Republic of China.

出版信息

J Inflamm Res. 2023 Jan 31;16:381-389. doi: 10.2147/JIR.S385977. eCollection 2023.

DOI:10.2147/JIR.S385977
PMID:36748023
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9899014/
Abstract

Ferroptosis is a recently identified iron-dependent form of intracellular lipid peroxide accumulation-mediated cell death. Different from other types of cell death mechanisms, it exhibits distinct biological and morphological features characterized by the loss of lipid peroxidase repair activity caused by glutathione peroxidase 4, the presence of redox-active iron, and the oxidation of phospholipids-containing polyunsaturated fatty acids. In recent years, studies have shown that ferroptosis plays a key role in various liver diseases such as alcoholic liver injury, non-alcoholic steatohepatitis, liver cirrhosis, and liver cancer. However, the mechanism of ferroptosis and its regulation on chronic liver disease are controversial among different types of cells in the liver. Herein, we summarize the current studies on mechanism of ferroptosis in chronic liver disease, aiming to outline the blueprint of ferroptosis as an effective option for chronic liver disease therapy.

摘要

铁死亡是一种最近被发现的、由细胞内脂质过氧化物积累介导的铁依赖性细胞死亡形式。与其他类型的细胞死亡机制不同,它表现出独特的生物学和形态学特征,其特征包括谷胱甘肽过氧化物酶4导致脂质过氧化物修复活性丧失、存在氧化还原活性铁以及含多不饱和脂肪酸的磷脂氧化。近年来,研究表明铁死亡在多种肝脏疾病如酒精性肝损伤、非酒精性脂肪性肝炎、肝硬化和肝癌中起关键作用。然而,在肝脏不同类型的细胞中,铁死亡的机制及其对慢性肝病的调节存在争议。在此,我们总结了目前关于慢性肝病中铁死亡机制的研究,旨在勾勒出铁死亡作为慢性肝病治疗有效选择的蓝图。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0303/9899014/fe4163045f75/JIR-16-381-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0303/9899014/4eb65f8617c2/JIR-16-381-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0303/9899014/fe4163045f75/JIR-16-381-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0303/9899014/4eb65f8617c2/JIR-16-381-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0303/9899014/fe4163045f75/JIR-16-381-g0002.jpg

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Ferroptosis of tumour neutrophils causes immune suppression in cancer.肿瘤中性粒细胞的铁死亡导致癌症中的免疫抑制。
Nature. 2022 Dec;612(7939):338-346. doi: 10.1038/s41586-022-05443-0. Epub 2022 Nov 16.
2
FNDC3B protects steatosis and ferroptosis via the AMPK pathway in alcoholic fatty liver disease.FNDC3B 通过 AMPK 通路在酒精性脂肪肝疾病中保护脂肪变性和铁死亡。
Free Radic Biol Med. 2022 Nov 20;193(Pt 2):808-819. doi: 10.1016/j.freeradbiomed.2022.10.322. Epub 2022 Nov 3.
3
Genetic variants in promoter region of is associated with the risk of non-alcoholic fatty liver disease in a Chinese Han population: a case-control study.
七叶皂苷钠通过ATF4/谷胱甘肽/谷胱甘肽过氧化物酶4轴介导的铁死亡诱导肝毒性。
Sci Rep. 2025 Jan 7;15(1):1141. doi: 10.1038/s41598-024-79723-2.
4
Ferroptosis as a promising targeted therapy for triple negative breast cancer.铁死亡作为一种有前途的三阴性乳腺癌靶向治疗策略。
Breast Cancer Res Treat. 2024 Oct;207(3):497-513. doi: 10.1007/s10549-024-07387-7. Epub 2024 Jun 14.
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Novel Therapeutic Approaches to Liver Fibrosis Based on Targeting Oxidative Stress.基于靶向氧化应激的肝纤维化新型治疗方法
Antioxidants (Basel). 2023 Aug 5;12(8):1567. doi: 10.3390/antiox12081567.
6
Treatment of liver fibrosis: Past, current, and future.肝纤维化的治疗:过去、现在与未来
World J Hepatol. 2023 Jun 27;15(6):755-774. doi: 10.4254/wjh.v15.i6.755.
在中国汉族人群中,[基因名称]启动子区域的遗传变异与非酒精性脂肪性肝病风险相关:一项病例对照研究。 (你原文中“of”后面缺少具体基因名称,请补充完整以便翻译更准确)
Gastroenterol Rep (Oxf). 2022 Oct 31;10:goac060. doi: 10.1093/gastro/goac060. eCollection 2022.
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Tanshinone functions as a coenzyme that confers gain of function of NQO1 to suppress ferroptosis.丹参酮作为辅酶发挥作用,赋予 NQO1 功能获得,从而抑制铁死亡。
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The gut microbiota metabolite glycochenodeoxycholate activates TFR-ACSL4-mediated ferroptosis to promote the development of environmental toxin-linked MAFLD.肠道微生物群代谢产物甘氨胆酸激活 TFR-ACSL4 介导的铁死亡,促进环境毒素相关 MAFLD 的发生发展。
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Inhibition of HSPA8 by rifampicin contributes to ferroptosis via enhancing autophagy.利福平通过抑制 HSPA8 促进自噬从而促进铁死亡。
Liver Int. 2022 Dec;42(12):2889-2899. doi: 10.1111/liv.15459. Epub 2022 Oct 26.
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