英國愛丁堡大學Will Wood小組發現,鐵死亡樣細胞死亡促進并延長果蠅的炎癥反應。相關論文于2024年6月25日在線發表于國際學術期刊《自然—細胞生物學》。
研究人人員利用活體成像技術發現了果蠅胚胎受傷時體內發生的一種獨特的、類似于鐵死亡的壞死性細胞死亡。研究人員進一步證明,巨噬細胞在胚胎內迅速與這些壞死細胞接觸,但卻難以將其吞噬,導致吞噬過程延長、受挫和死亡細胞頻繁解體。相反,在創傷過程中抑制鐵死亡程序會延遲巨噬細胞被招募到損傷部位,這表明鐵死亡在體內炎癥過程中扮演著相互沖突的角色。
據介紹,鐵死亡是一種獨特的細胞壞死形式,由大量脂質過氧化引起,新出現的證據表明,鐵死亡在多種病癥的器官損傷中起著重要作用。然而,由于缺乏特異性探針,鐵死亡尚未在體內可視化,這嚴重限制了對免疫系統如何與鐵死亡細胞相互作用以及這一過程如何導致炎癥的研究。因此,鐵死亡是否具有生理作用仍然是一個懸而未決的關鍵問題。
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—細胞生物學》,創刊于1999年。隸屬于施普林格·自然出版集團,最新IF:28.213
官方網址:https://www.nature.com/ncb
投稿鏈接:https://mts-ncb.nature.com/cgi-bin/main.plex
美鳳力借多年的大動物經驗,堅持以“務實求真”為宗旨,累計為4000多家客戶提供品質大動物臨床前服務,得到了客戶的一致好評。如果您有動物試驗、臨床培訓、組織病理、大動物試驗、臨床試驗、產品注冊科研課題等...
請立即點擊咨詢我們或撥打咨詢熱線: 17312606166 ,我們會詳細為你一一解答你心中的疑難。 添加好友