Ferroptosis: past, present and future

• Published in: Cell death & disease Vol. 11; no. 2; p. 88
• Main Authors: Li, Jie, Cao, Feng, Yin, He-liang, Huang, Zi-jian, Lin, Zhi-tao, Mao, Ning, Sun, Bei, Wang, Gang
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 03-02-2020; Springer Nature B.V
• Subjects: 631/80/82; 631/80/86; Acute Kidney Injury - drug therapy; Acute Kidney Injury - pathology; Antibodies; Antioxidants; Antioxidants - metabolism; Apoptosis; Biochemistry; Biomedical and Life Sciences; Cell Biology; Cell Culture; Cell death; Cell Death - drug effects; Cell Death - physiology; Ferroptosis; Ferroptosis - drug effects; Ferroptosis - physiology; Glutathione peroxidase; Hematological diseases; Immunology; Iron; Iron - metabolism; Ischemia; Life Sciences; Lipid Metabolism; Lipid Peroxidation; Molecular modelling; Neoplasms - drug therapy; Neoplasms - pathology; Nervous system; Nervous system diseases; Nervous System Diseases - drug therapy; Nervous System Diseases - pathology; Reactive oxygen species; Reperfusion; Reperfusion Injury - drug therapy; Reperfusion Injury - pathology; Review; Review Article; Tumors
• ISSN: 2041-4889; 2041-4889
• DOI: 10.1038/s41419-020-2298-2

Ferroptosis is a new type of cell death that was discovered in recent years and is usually accompanied by a large amount of iron accumulation and lipid peroxidation during the cell death process; the occurrence of ferroptosis is iron-dependent. Ferroptosis-inducing factors can directly or indirectly affect glutathione peroxidase through different pathways, resulting in a decrease in antioxidant capacity and accumulation of lipid reactive oxygen species (ROS) in cells, ultimately leading to oxidative cell death. Recent studies have shown that ferroptosis is closely related to the pathophysiological processes of many diseases, such as tumors, nervous system diseases, ischemia-reperfusion injury, kidney injury, and blood diseases. How to intervene in the occurrence and development of related diseases by regulating cell ferroptosis has become a hotspot and focus of etiological research and treatment, but the functional changes and specific molecular mechanisms of ferroptosis still need to be further explored. This paper systematically summarizes the latest progress in ferroptosis research, with a focus on providing references for further understanding of its pathogenesis and for proposing new targets for the treatment of related diseases.