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铁死亡的机制及其在脊髓损伤中的作用

Mechanism of Ferroptosis and Its Role in Spinal Cord Injury.

作者信息

Li Fei, Wang Haifan, Chen Hao, Guo Jianing, Dang Xiaoqian, Ru Yi, Wang Haoyu

机构信息

Department of Orthopedics, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.

Basic Medical Science Academy, The Air Force Medical University, Xi'an, China.

出版信息

Front Neurol. 2022 Jun 9;13:926780. doi: 10.3389/fneur.2022.926780. eCollection 2022.

DOI:10.3389/fneur.2022.926780
PMID:35756929
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9218271/
Abstract

Ferroptosis is a non-necrotic form of regulated cell death (RCD) that is primarily characterized by iron-dependent membrane lipid peroxidation and is regulated by cysteine transport, glutathione synthesis, and glutathione peroxidase 4 function as well as other proteins including ferroptosis suppressor protein 1. It has been found that ferroptosis played an important role in many diseases, such as neurodegenerative diseases and ischemia-reperfusion injury. Spinal cord injury (SCI), especially traumatic SCI, is an urgent problem worldwide due to its high morbidity and mortality, as well as the destruction of functions of the human body. Various RCDs, including ferroptosis, are found in SCI. Different from necrosis, since RCD is a form of cell death regulated by various molecular mechanisms in cells, the study of the role played by RCD in SCI will contribute to a deeper understanding of the pathophysiological process, as well as the treatment and functional recovery. The present review mainly introduces the main mechanism of ferroptosis and its role in SCI, so as to provide a new idea for further exploration.

摘要

铁死亡是一种程序性细胞死亡(RCD)的非坏死形式,其主要特征是铁依赖性膜脂质过氧化,并受半胱氨酸转运、谷胱甘肽合成、谷胱甘肽过氧化物酶4功能以及包括铁死亡抑制蛋白1在内的其他蛋白质调控。研究发现,铁死亡在许多疾病中发挥重要作用,如神经退行性疾病和缺血再灌注损伤。脊髓损伤(SCI),尤其是创伤性SCI,因其高发病率和死亡率以及对人体功能的破坏,是全球范围内的一个紧迫问题。在SCI中发现了包括铁死亡在内的各种程序性细胞死亡。与坏死不同,由于程序性细胞死亡是细胞内各种分子机制调控的细胞死亡形式,研究程序性细胞死亡在SCI中的作用将有助于更深入地了解病理生理过程以及治疗和功能恢复。本综述主要介绍铁死亡的主要机制及其在SCI中的作用,以期为进一步探索提供新思路。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8fcc/9218271/b7285eb2c949/fneur-13-926780-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8fcc/9218271/96d9d5745777/fneur-13-926780-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8fcc/9218271/251bbd9cbec8/fneur-13-926780-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8fcc/9218271/b7285eb2c949/fneur-13-926780-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8fcc/9218271/96d9d5745777/fneur-13-926780-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8fcc/9218271/251bbd9cbec8/fneur-13-926780-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8fcc/9218271/b7285eb2c949/fneur-13-926780-g0003.jpg

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Mol Cancer. 2022 Jan 4;21(1):11. doi: 10.1186/s12943-021-01466-9.
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Front Immunol. 2025 Jul 10;16:1574834. doi: 10.3389/fimmu.2025.1574834. eCollection 2025.
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