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铁死亡的分子机制及其在慢性阻塞性肺疾病中的作用。

The molecular mechanism of ferroptosis and its role in COPD.

作者信息

Meng Dandan, Zhu Chengfeng, Jia Ruixue, Li Zongxin, Wang Wantao, Song Suhua

机构信息

Department of Traditional Chinese Medicine, Shandong University of Traditional Chinese Medicine, Jinan, China.

Department of Second Department of Haematology, Jinan Haematology Hospital, Jinan, China.

出版信息

Front Med (Lausanne). 2023 Jan 6;9:1052540. doi: 10.3389/fmed.2022.1052540. eCollection 2022.

Abstract

Ferroptosis, a new type of cell death, is mainly characterized by intracellular iron accumulation and lipid peroxidation. The complex regulatory network of iron metabolism, lipid metabolism, amino acid metabolism, p53-related signaling, and Nrf2-related signaling factors is involved in the entire process of ferroptosis. It has been reported that ferroptosis is involved in the pathogenesis of neurological diseases, cancer, and ischemia-reperfusion injury. Recent studies found that ferroptosis is closely related to the pathogenesis of COPD, which, to some extent, indicates that ferroptosis is a potential therapeutic target for COPD. This article mainly discusses the related mechanisms of ferroptosis, including metabolic regulation and signaling pathway regulation, with special attention to its role in the pathogenesis of COPD, aiming to provide safe and effective therapeutic targets for chronic airway inflammatory diseases.

摘要

铁死亡是一种新型细胞死亡方式,主要特征为细胞内铁蓄积和脂质过氧化。铁代谢、脂质代谢、氨基酸代谢、p53相关信号及Nrf2相关信号因子的复杂调控网络参与了铁死亡的全过程。据报道,铁死亡参与了神经疾病、癌症及缺血再灌注损伤的发病机制。近期研究发现,铁死亡与慢性阻塞性肺疾病(COPD)的发病机制密切相关,这在一定程度上表明铁死亡是COPD的一个潜在治疗靶点。本文主要探讨铁死亡的相关机制,包括代谢调控和信号通路调控,特别关注其在COPD发病机制中的作用,旨在为慢性气道炎症性疾病提供安全有效的治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ecf7/9852995/324aad0f52a4/fmed-09-1052540-g0001.jpg

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