英国爱丁堡大学Will Wood小组发现，铁死亡样细胞死亡促进并延长果蝇的炎症反应。相关论文于2024年6月25日在线发表于国际学术期刊《自然—细胞生物学》。

研究人人员利用活体成像技术发现了果蝇胚胎受伤时体内发生的一种独特的、类似于铁死亡的坏死性细胞死亡。研究人员进一步证明，巨噬细胞在胚胎内迅速与这些坏死细胞接触，但却难以将其吞噬，导致吞噬过程延长、受挫和死亡细胞频繁解体。相反，在创伤过程中抑制铁死亡程序会延迟巨噬细胞被招募到损伤部位，这表明铁死亡在体内炎症过程中扮演着相互冲突的角色。

据介绍，铁死亡是一种独特的细胞坏死形式，由大量脂质过氧化引起，新出现的证据表明，铁死亡在多种病症的器官损伤中起着重要作用。然而，由于缺乏特异性探针，铁死亡尚未在体内可视化，这严重限制了对免疫系统如何与铁死亡细胞相互作用以及这一过程如何导致炎症的研究。因此，铁死亡是否具有生理作用仍然是一个悬而未决的关键问题。

附：英文原文

Title: Ferroptosis-like cell death promotes and prolongs inflammation in Drosophila

Author: Davidson, Andrew J., Heron, Rosalind, Das, Jyotirekha, Overholtzer, Michael, Wood, Will

Issue&Volume: 2024-06-25

Abstract: Ferroptosis is a distinct form of necrotic cell death caused by overwhelming lipid peroxidation, and emerging evidence indicates a major contribution to organ damage in multiple pathologies. However, ferroptosis has not yet been visualized in vivo due to a lack of specific probes, which has severely limited the study of how the immune system interacts with ferroptotic cells and how this process contributes to inflammation. Consequently, whether ferroptosis has a physiological role has remained a key outstanding question. Here we identify a distinct, ferroptotic-like, necrotic cell death occurring in vivo during wounding of the Drosophila embryo using live imaging. We further demonstrate that macrophages rapidly engage these necrotic cells within the embryo but struggle to engulf them, leading to prolonged, frustrated phagocytosis and frequent corpse disintegration. Conversely, suppression of the ferroptotic programme during wounding delays macrophage recruitment to the injury site, pointing to conflicting roles for ferroptosis during inflammation in vivo.

DOI: 10.1038/s41556-024-01450-7

Source: https://www.nature.com/articles/s41556-024-01450-7

期刊信息

Nature Cell Biology：《自然—细胞生物学》，创刊于1999年。隶属于施普林格·自然出版集团，最新IF：28.213

官方网址：https://www.nature.com/ncb

投稿链接：https://mts-ncb.nature.com/cgi-bin/main.plex