ISSN: 1449-2288International Journal of Biological Sciences
Global reach, higher impact
Int J Biol Sci 2023; 19(9):2756-2771. doi:10.7150/ijbs.83348 This issue Cite
Review
The crosstalk between ferroptosis and mitochondrial dynamic regulatory networks
1. Department of General Surgery, Xuanwu Hospital, Capital Medical University, Beijing, China.
2. Clinical Center for Acute Pancreatitis, Capital Medical University, Beijing, China.
* These authors contributed equally to this paper.
Abstract
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.
Keywords: ferroptosis, reactive oxygen species, mitochondrial homeostasis, mitochondrial fission, mitochondrial fusion, mitophagy
Citation styles
