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铁死亡的分子机制及其与急性肾损伤的关系

Molecular Mechanisms of Ferroptosis and Their Involvement in Acute Kidney Injury.

作者信息

Liu Jie, Han Xiaoxia, Zhou Jia, Leng Yufang

机构信息

The First School of Clinical Medicine, Lanzhou University, Lanzhou, People's Republic of China.

Department of Anesthesiology, The First Hospital of Lanzhou University, Lanzhou, People's Republic of China.

出版信息

J Inflamm Res. 2023 Nov 2;16:4941-4951. doi: 10.2147/JIR.S427505. eCollection 2023.

DOI:10.2147/JIR.S427505
PMID:37936596
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10627075/
Abstract

Ferroptosis is a novel way of regulating cell death, which occurs in a process that is closely linked to intracellular iron metabolism, lipid metabolism, amino acid metabolism, and multiple signaling pathways. The latest research shows that ferroptosis plays a key role in the pathogenesis of acute kidney injury (AKI). Ferroptosis may be an important target for treating AKI caused by various reasons, such as ischemia-reperfusion injury, rhabdomyolysis syndrome, sepsis, and nephrotoxic drugs. This paper provides a review on the regulatory mechanisms of ferroptosis and its role in AKI, which may help to provide new research ideas for the treatment of AKI and future research.

摘要

铁死亡是一种调节细胞死亡的新方式,其发生过程与细胞内铁代谢、脂质代谢、氨基酸代谢及多种信号通路密切相关。最新研究表明,铁死亡在急性肾损伤(AKI)的发病机制中起关键作用。铁死亡可能是治疗由各种原因引起的AKI的重要靶点,如缺血再灌注损伤、横纹肌溶解综合征、脓毒症和肾毒性药物。本文对铁死亡的调控机制及其在AKI中的作用进行综述,这可能有助于为AKI的治疗及未来研究提供新的研究思路。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2c6b/10627075/ea1ce2cebe02/JIR-16-4941-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2c6b/10627075/1c8ef3b12aa0/JIR-16-4941-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2c6b/10627075/ea1ce2cebe02/JIR-16-4941-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2c6b/10627075/1c8ef3b12aa0/JIR-16-4941-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2c6b/10627075/ea1ce2cebe02/JIR-16-4941-g0002.jpg

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本文引用的文献

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vPIF-1 is an insulin-like antiferroptotic viral peptide.vPIF-1 是一种类胰岛素抗铁死亡的病毒肽。
Proc Natl Acad Sci U S A. 2023 May 23;120(21):e2300320120. doi: 10.1073/pnas.2300320120. Epub 2023 May 15.
2
Renal Clearable Quantum Dot-Drug Conjugates Modulate Labile Iron Species and Scavenge Free Radicals for Attenuating Chemotherapeutic Drug-Induced Acute Kidney Injury.肾脏可清除的量子点-药物偶联物调节不稳定铁物种并清除自由基,以减轻化疗药物引起的急性肾损伤。
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Cyanidin-3-glucoside inhibits ferroptosis in renal tubular cells after ischemia/reperfusion injury via the AMPK pathway.
Cell Mol Life Sci. 2025 Apr 2;82(1):138. doi: 10.1007/s00018-025-05666-0.
矢车菊素-3-葡萄糖苷通过 AMPK 通路抑制缺血再灌注损伤后肾小管细胞中的铁死亡。
Mol Med. 2023 Apr 3;29(1):42. doi: 10.1186/s10020-023-00642-5.
4
A Preclinical Model for Parkinson's Disease Based on Transcriptional Gene Activation via KEAP1/NRF2 to Develop New Antioxidant Therapies.一种基于通过KEAP1/NRF2激活转录基因来开发新的抗氧化疗法的帕金森病临床前模型。
Antioxidants (Basel). 2023 Mar 9;12(3):673. doi: 10.3390/antiox12030673.
5
TRIM21 ubiquitylates GPX4 and promotes ferroptosis to aggravate ischemia/reperfusion-induced acute kidney injury.TRIM21 泛素化 GPX4 并促进铁死亡以加重缺血/再灌注引起的急性肾损伤。
Life Sci. 2023 May 15;321:121608. doi: 10.1016/j.lfs.2023.121608. Epub 2023 Mar 21.
6
Mitophagy alleviates cisplatin-induced renal tubular epithelial cell ferroptosis through ROS/HO-1/GPX4 axis.线粒体自噬通过 ROS/HO-1/GPX4 轴缓解顺铂诱导的肾小管上皮细胞铁死亡。
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Allergol Immunopathol (Madr). 2023 Mar 1;51(2):99-110. doi: 10.15586/aei.v51i2.760. eCollection 2023.
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