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消除铁死亡在免疫中的作用。

Ironing out the role of ferroptosis in immunity.

机构信息

Department of Surgery, University of Michigan School of Medicine, Ann Arbor, MI, USA; Center of Excellence for Cancer Immunology and Immunotherapy, University of Michigan School of Medicine, Rogel Cancer Center, Ann Arbor, MI, USA; Graduate Program in Cancer Biology, University of Michigan, Ann Arbor, MI, USA; Graduate Program in Immunology, University of Michigan, Ann Arbor, MI, USA.

Department of Biological Sciences, Department of Chemistry, Department of Pathology and Cell Biology, Herbert Irving Comprehensive Cancer Center, Columbia University, New York, NY, USA.

出版信息

Immunity. 2024 May 14;57(5):941-956. doi: 10.1016/j.immuni.2024.03.019.

DOI:10.1016/j.immuni.2024.03.019
PMID:38749397
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11101142/
Abstract

Ferroptosis is a type of regulated cell death that drives the pathophysiology of many diseases. Oxidative stress is detectable in many types of regulated cell death, but only ferroptosis involves lipid peroxidation and iron dependency. Ferroptosis originates and propagates from several organelles, including the mitochondria, endoplasmic reticulum, Golgi, and lysosomes. Recent data have revealed that immune cells can both induce and undergo ferroptosis. A mechanistic understanding of how ferroptosis regulates immunity is critical to understanding how ferroptosis controls immune responses and how this is dysregulated in disease. Translationally, more work is needed to produce ferroptosis-modulating immunotherapeutics. This review focuses on the role of ferroptosis in immune-related diseases, including infection, autoimmune diseases, and cancer. We discuss how ferroptosis is regulated in immunity, how this regulation contributes to disease pathogenesis, and how targeting ferroptosis may lead to novel therapies.

摘要

铁死亡是一种调节性细胞死亡,它驱动着许多疾病的病理生理学。氧化应激在许多类型的调节性细胞死亡中都能检测到,但只有铁死亡涉及脂质过氧化和铁依赖性。铁死亡起源于并从多个细胞器传播,包括线粒体、内质网、高尔基体和溶酶体。最近的数据表明,免疫细胞既可以诱导也可以经历铁死亡。对铁死亡如何调节免疫的机制理解对于理解铁死亡如何控制免疫反应以及在疾病中如何失调至关重要。在翻译方面,需要做更多的工作来产生铁死亡调节免疫疗法。这篇综述集中讨论了铁死亡在与免疫相关的疾病中的作用,包括感染、自身免疫性疾病和癌症。我们讨论了铁死亡在免疫中的调节方式,这种调节如何导致疾病的发病机制,以及靶向铁死亡可能导致新的治疗方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f344/11101142/8b975a0454f9/nihms-1984408-f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f344/11101142/aad14d21f88c/nihms-1984408-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f344/11101142/3988d3411fba/nihms-1984408-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f344/11101142/e911cc1bbd93/nihms-1984408-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f344/11101142/8b975a0454f9/nihms-1984408-f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f344/11101142/aad14d21f88c/nihms-1984408-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f344/11101142/3988d3411fba/nihms-1984408-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f344/11101142/e911cc1bbd93/nihms-1984408-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f344/11101142/8b975a0454f9/nihms-1984408-f0004.jpg

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本文引用的文献

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7-Dehydrocholesterol is an endogenous suppressor of ferroptosis.7-脱氢胆固醇是一种内源性的铁死亡抑制剂。
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Neutrophils resist ferroptosis and promote breast cancer metastasis through aconitate decarboxylase 1.中性粒细胞通过 aconitate decarboxylase 1 抵抗铁死亡并促进乳腺癌转移。
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