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铁死亡在系统性红斑狼疮中的潜在作用。

The Potential Role of Ferroptosis in Systemic Lupus Erythematosus.

机构信息

Department of Dermatology, Huashan Hospital, Fudan University, Shanghai, China.

出版信息

Front Immunol. 2022 Apr 21;13:855622. doi: 10.3389/fimmu.2022.855622. eCollection 2022.

DOI:10.3389/fimmu.2022.855622
PMID:35529869
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9068945/
Abstract

Systemic lupus erythematosus (SLE) is an autoimmune disease that is accompanied with autoantibody production and inflammation. Other features of SLE pathogenesis include iron accumulation, oxidative stress, and lipid peroxidation, which are also major biochemical characteristics of ferroptosis, a novel non-apoptotic regulated form of cell death. To date, ferroptosis has been demonstrated to be an important driver of lupus progression, and several ferroptosis inhibitors have therapeutic effect in lupus-prone mice. Given the emerging link between ferroptosis and SLE, it can be postulated that ferroptosis is an integral component in the vicious cycle of immune dysfunction, inflammation, and tissue damage in SLE pathogenesis. In this review, we summarize the potential links between ferroptosis and SLE, with the aim of elucidating the underlying pathogenic mechanism of ferroptosis in lupus, and providing a new promising therapeutic strategy for SLE.

摘要

系统性红斑狼疮(SLE)是一种自身免疫性疾病,伴有自身抗体的产生和炎症。SLE 发病机制的其他特征还包括铁积累、氧化应激和脂质过氧化,这些也是铁死亡这一新型非凋亡调控细胞死亡形式的主要生化特征。迄今为止,铁死亡已被证明是狼疮进展的重要驱动因素,几种铁死亡抑制剂在狼疮易感小鼠中具有治疗作用。鉴于铁死亡与 SLE 之间的新联系,可以推测铁死亡是 SLE 发病机制中免疫功能障碍、炎症和组织损伤的恶性循环中的一个组成部分。在这篇综述中,我们总结了铁死亡与 SLE 之间的潜在联系,旨在阐明铁死亡在狼疮中的潜在发病机制,并为 SLE 提供一种有前景的新治疗策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/44b3/9068945/67226c13cd98/fimmu-13-855622-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/44b3/9068945/9a8c1c549324/fimmu-13-855622-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/44b3/9068945/67226c13cd98/fimmu-13-855622-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/44b3/9068945/9a8c1c549324/fimmu-13-855622-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/44b3/9068945/67226c13cd98/fimmu-13-855622-g002.jpg

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本文引用的文献

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Redox Biol. 2021 Nov;47:102143. doi: 10.1016/j.redox.2021.102143. Epub 2021 Sep 25.
2
Glutathione peroxidase 4-regulated neutrophil ferroptosis induces systemic autoimmunity.谷胱甘肽过氧化物酶4调节的中性粒细胞铁死亡诱导全身自身免疫。
Nat Immunol. 2021 Sep;22(9):1107-1117. doi: 10.1038/s41590-021-00993-3. Epub 2021 Aug 12.
3
Differential sensitivity of inflammatory macrophages and alternatively activated macrophages to ferroptosis.
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J Inflamm Res. 2025 Mar 14;18:3859-3878. doi: 10.2147/JIR.S500115. eCollection 2025.
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Exploring mitochondrial and ferroptotic mechanisms for systemic lupus erythematosus biomarker identification and therapy.探索线粒体和铁死亡机制以用于系统性红斑狼疮生物标志物的识别与治疗。
Sci Rep. 2025 Mar 17;15(1):9140. doi: 10.1038/s41598-025-93872-y.
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Intricating connections: the role of ferroptosis in systemic lupus erythematosus.错综复杂的联系:铁死亡在系统性红斑狼疮中的作用
Front Immunol. 2025 Feb 4;16:1534926. doi: 10.3389/fimmu.2025.1534926. eCollection 2025.
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