Wickert Anja, Schwantes Anna, Fuhrmann Dominik C, Brüne Bernhard
Institute of Biochemistry I, Faculty of Medicine, Goethe University Frankfurt, Frankfurt, Germany.
German Cancer Consortium (DKTK), Partner Site Frankfurt, Frankfurt, Germany.
Front Pharmacol. 2024 Sep 20;15:1474285. doi: 10.3389/fphar.2024.1474285. eCollection 2024.
Ferroptosis is an iron-dependent form of cell death, which finally culminates in lipid peroxidation and membrane damage. During the past decade, the interest in ferroptosis increased substantially and various regulatory components were discovered. The role of ferroptosis during inflammation and its impact on different immune cell populations is still under debate. Activation of inflammatory pathways such as nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and hypoxia inducible factors (HIFs) are known to alter the ability of cells to undergo ferroptosis and are closely connected to iron metabolism. During inflammation, iron regulatory systems fundamentally change and cells such as macrophages and neutrophils adapt their metabolism towards iron sequestering phenotypes. In this review, we discuss how ferroptosis alters inflammatory pathways and how iron metabolism under inflammatory conditions affects immune cell ferroptosis.
铁死亡是一种铁依赖性的细胞死亡形式,最终以脂质过氧化和膜损伤告终。在过去十年中,人们对铁死亡的兴趣大幅增加,并且发现了各种调节成分。铁死亡在炎症过程中的作用及其对不同免疫细胞群体的影响仍存在争议。已知激活炎症途径,如活化B细胞的核因子κB轻链增强子(NF-κB)和缺氧诱导因子(HIFs),会改变细胞发生铁死亡的能力,并且与铁代谢密切相关。在炎症过程中,铁调节系统发生根本性变化,巨噬细胞和中性粒细胞等细胞会使其代谢适应铁螯合表型。在这篇综述中,我们讨论了铁死亡如何改变炎症途径,以及炎症条件下的铁代谢如何影响免疫细胞铁死亡。