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The crosstalk between ferroptosis and mitochondrial dynamic regulatory networks

期刊

INTERNATIONAL JOURNAL OF BIOLOGICAL SCIENCES
卷 19, 期 9, 页码 2756-2771

出版社

IVYSPRING INT PUBL
DOI: 10.7150/ijbs.83348

关键词

ferroptosis; reactive oxygen species; mitochondrial homeostasis; mitochondrial fission; mitochondrial fusion; mitophagy

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Ferroptosis is a form of cell death characterized by iron accumulation and excessive lipid peroxidation, which is closely associated with mitochondrial function. Mitochondrial dysfunction and damage promote oxidative stress, leading to ferroptosis. Abnormalities in mitochondrial morphology and function are closely linked to the development of various diseases. Mitochondrial homeostasis is regulated through processes such as fission, fusion, and mitophagy, which are also intimately related to ferroptosis. Understanding the dynamic regulation of mitochondrial processes during ferroptosis is crucial for studying disease development.
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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