The crosstalk between ferroptosis and mitochondrial dynamic regulatory networks

粒体自噬 线粒体融合 线粒体分裂 串扰 线粒体 氧化应激 程序性细胞死亡 功能(生物学) 细胞生物学 生物 线粒体DNA 细胞凋亡 遗传学 自噬 生物化学 基因 光学 物理
作者
Jie Li,Yuchen Jia,Yi-xuan Ding,Jian Bai,Feng Cao,Fei Li
出处
期刊:International Journal of Biological Sciences [Ivyspring International Publisher]
卷期号:19 (9): 2756-2771 被引量:93
标识
DOI:10.7150/ijbs.83348
摘要

Ferroptosis is an iron-driven cell death modality characterized by iron accumulation and excessive lipid peroxidation.Ferroptosis is closely related to mitochondrial function, as indicated by studies showing that mitochondrial dysfunction and damage promote oxidative stress, which in turn induces ferroptosis.Mitochondria play crucial roles in cellular homeostasis, and abnormalities in their morphology and function are closely associated with the development of many diseases.Mitochondria are highly dynamic organelles, and their stability is maintained through a series of regulatory pathways.Mitochondrial homeostasis is dynamically regulated, mainly via key processes such as mitochondrial fission, mitochondrial fusion and mitophagy; however, mitochondrial processes are prone to dysregulation.Mitochondrial fission and fusion and mitophagy are intimately related to ferroptosis.Therefore, investigations into the dynamic regulation of mitochondrial processes during ferroptosis are important to provide a better understanding of the development of disease.In this paper, we systematically summarized changes in ferroptosis, mitochondrial fission and fusion and mitophagy to promote an in-depth understanding of the mechanism underlying ferroptosis and provide a corresponding reference for the treatment of related diseases.
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