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器官缺血再灌注损伤中的铁死亡:最新进展与策略

Ferroptosis in organ ischemia-reperfusion injuries: recent advancements and strategies.

作者信息

Luan Xiaoyu, Chen Peng, Miao Longyu, Yuan Xinying, Yu Chaoqun, Di Guohu

机构信息

School of Basic Medicine, Qingdao University, 308 Ningxia Road, Qingdao, 266071, China.

Institute of Stem Cell and Regenerative Medicine, School of Basic Medicine, Qingdao University, Qingdao, China.

出版信息

Mol Cell Biochem. 2025 Jan;480(1):19-41. doi: 10.1007/s11010-024-04978-2. Epub 2024 Mar 31.

DOI:10.1007/s11010-024-04978-2
PMID:38556592
Abstract

Ferroptosis is a newly discovered type of regulated cell death participated in multiple diseases. Different from other classical cell death programs such as necrosis and apoptosis, ferroptosis involving iron-catalyzed lipid peroxidation is characterized by Fe accumulation and mitochondria alterations. The phenomenon of oxidative stress following organ ischemia-reperfusion (I/R) has recently garnered attention for its connection to the onset of ferroptosis and subsequent reperfusion injuries. This article provides a comprehensive overview underlying the mechanisms of ferroptosis, with a further focus on the latest research progress regarding interference with ferroptotic pathways in organ I/R injuries, such as intestine, lung, heart, kidney, liver, and brain. Understanding the links between ferroptosis and I/R injury may inform potential therapeutic strategies and targeted agents.

摘要

铁死亡是一种新发现的参与多种疾病的程序性细胞死亡。与坏死和凋亡等其他经典细胞死亡程序不同,铁死亡涉及铁催化的脂质过氧化,其特征是铁积累和线粒体改变。器官缺血再灌注(I/R)后的氧化应激现象最近因其与铁死亡的发生及随后的再灌注损伤的关联而受到关注。本文全面概述了铁死亡的机制,并进一步聚焦于在肠道、肺、心脏、肾脏、肝脏和大脑等器官I/R损伤中干扰铁死亡途径的最新研究进展。了解铁死亡与I/R损伤之间的联系可能为潜在的治疗策略和靶向药物提供依据。

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Ferroptosis in organ ischemia-reperfusion injuries: recent advancements and strategies.器官缺血再灌注损伤中的铁死亡:最新进展与策略
Mol Cell Biochem. 2025 Jan;480(1):19-41. doi: 10.1007/s11010-024-04978-2. Epub 2024 Mar 31.
2
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SIRT4-Mediated Deacetylation of PRDX3 Attenuates Liver Ischemia Reperfusion Injury by Suppressing Ferroptosis.SIRT4介导的PRDX3去乙酰化通过抑制铁死亡减轻肝脏缺血再灌注损伤。
Int J Biol Sci. 2025 Jul 11;21(10):4663-4682. doi: 10.7150/ijbs.114510. eCollection 2025.
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Mitochondrial Ferritin Overexpression Attenuates Ferroptosis and Mitochondrial Dysfunction by Reducing VDAC1 to Relieve MI/RI-Induced Damage.

本文引用的文献

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Comprehensive Pan-Cancer Mutation Density Patterns in Enhancer RNA.增强子 RNA 中的全面泛癌突变密度模式
Int J Mol Sci. 2023 Dec 30;25(1):534. doi: 10.3390/ijms25010534.
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Filamentous-Actin-Mimicking Nanoplatform for Enhanced Cytosolic Protein Delivery.纤维状肌动蛋白模拟纳米平台用于增强细胞溶质蛋白递送。
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线粒体铁蛋白过表达通过降低电压依赖性阴离子通道1(VDAC1)减轻铁死亡和线粒体功能障碍,从而缓解心肌缺血/再灌注损伤。
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Electroacupuncture Attenuates Cerebral Ischemia-Reperfusion Injury by Inhibiting Ferroptosis via the p53/SLC7A11 Pathway.电针通过p53/SLC7A11通路抑制铁死亡减轻脑缺血再灌注损伤
Clin Exp Pharmacol Physiol. 2025 May;52(5):e70036. doi: 10.1111/1440-1681.70036.
6
Iron chelators loaded on myocardiocyte mitochondria-targeted nanozyme system for treating myocardial ischemia-reperfusion injury in mouse models.负载于心肌细胞线粒体靶向纳米酶系统的铁螯合剂用于治疗小鼠模型中的心肌缺血再灌注损伤。
J Nanobiotechnology. 2025 Feb 15;23(1):112. doi: 10.1186/s12951-025-03197-1.
7
Based on bioinformatics, SESN2 negatively regulates ferroptosis induced by ischemia reperfusion via the System Xc-/GPX4 pathway.基于生物信息学分析,SESN2通过System Xc-/GPX4途径负向调控缺血再灌注诱导的铁死亡。
Front Genet. 2025 Jan 29;15:1504114. doi: 10.3389/fgene.2024.1504114. eCollection 2024.
8
The role of ferroptosis in liver injury after cold ischemia-reperfusion in rats with autologous orthotopic liver transplantation.铁死亡在大鼠自体原位肝移植冷缺血再灌注后肝损伤中的作用
J Artif Organs. 2025 Jan 6. doi: 10.1007/s10047-024-01488-2.
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Cell Death Discov. 2024 Sep 10;10(1):401. doi: 10.1038/s41420-024-02169-y.
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β-氨基异丁酸是支链氨基酸的代谢物,可激活 AMPK/Nrf-2 通路,防止铁死亡,改善肺缺血再灌注损伤。
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Sci Rep. 2023 Oct 11;13(1):17212. doi: 10.1038/s41598-023-44249-6.
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Liproxstatin-1 Alleviates Lung Transplantation-induced Cold Ischemia-Reperfusion Injury by Inhibiting Ferroptosis.脂氧素A1通过抑制铁死亡减轻肺移植诱导的冷缺血-再灌注损伤。
Transplantation. 2023 Oct 1;107(10):2190-2202. doi: 10.1097/TP.0000000000004638. Epub 2023 May 19.
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Int Immunopharmacol. 2023 Feb;115:109731. doi: 10.1016/j.intimp.2023.109731. Epub 2023 Jan 20.