线粒体介导的自由基引发的铁死亡在疾病治疗中的作用机制及其意义
Mitochondria-mediated Ferroptosis in Diseases Therapy: From Molecular Mechanisms to Implications.
发表日期:2023 Jul 28
作者:
Fuhai Feng, Shasha He, Xiaoling Li, Jiake He, Lianxiang Luo
来源:
Cellular & Molecular Immunology
摘要:
铁死灭是一种涉及铁和脂质过氧化反应的细胞死亡方式,已被发现与许多疾病的发展密切相关。线粒体是真核细胞的重要组成部分,在能量生成、细胞代谢和凋亡调节中起着重要作用。目前,线粒体与铁死灭之间的确切关系尚不清楚。本研究旨在从多个角度系统阐明线粒体调节铁死灭的机制,以提供线粒体在铁死灭中的新见解。此外,我们还全面概述了线粒体在不同情况下,包括癌症、心血管疾病、炎症性疾病、线粒体DNA耗竭综合征和新型冠状病毒肺炎中对铁死灭的贡献。对线粒体参与铁死灭的全面了解可为基础细胞生物学研究和医学治疗提供更有效的方法。
Ferroptosis, a type of cell death involving iron and lipid peroxidation, has been found to be closely associated with the development of many diseases. Mitochondria are vital components of eukaryotic cells, serving important functions in energy production, cellular metabolism, and apoptosis regulation. Presently, the precise relationship between mitochondria and ferroptosis remains unclear. In this study, we aim to systematically elucidate the mechanisms via which mitochondria regulate ferroptosis from multiple perspectives to provide novel insights into mitochondrial functions in ferroptosis. Additionally, we present a comprehensive overview of how mitochondria contribute to ferroptosis in different conditions, including cancer, cardiovascular disease, inflammatory disease, mitochondrial DNA depletion syndrome, and novel coronavirus pneumonia. Gaining a comprehensive understanding of the involvement of mitochondria in ferroptosis could lead to more effective approaches for both basic cell biology studies and medical treatments.