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Ferroptosis: mechanisms and links with diseases
- Source :
- Signal Transduction and Targeted Therapy, Signal Transduction and Targeted Therapy, Vol 6, Iss 1, Pp 1-16 (2021)
- Publication Year :
- 2021
- Publisher :
- Springer Science and Business Media LLC, 2021.
-
Abstract
- Ferroptosis is an iron-dependent cell death, which is different from apoptosis, necrosis, autophagy, and other forms of cell death. The process of ferroptotic cell death is defined by the accumulation of lethal lipid species derived from the peroxidation of lipids, which can be prevented by iron chelators (e.g., deferiprone, deferoxamine) and small lipophilic antioxidants (e.g., ferrostatin, liproxstatin). This review summarizes current knowledge about the regulatory mechanism of ferroptosis and its association with several pathways, including iron, lipid, and cysteine metabolism. We have further discussed the contribution of ferroptosis to the pathogenesis of several diseases such as cancer, ischemia/reperfusion, and various neurodegenerative diseases (e.g., Alzheimer’s disease and Parkinson’s disease), and evaluated the therapeutic applications of ferroptosis inhibitors in clinics.
- Subjects :
- 0301 basic medicine
Cell biology
Cancer Research
Programmed cell death
Necrosis
Iron
lcsh:Medicine
Apoptosis
Review Article
Disease
Pathogenesis
03 medical and health sciences
chemistry.chemical_compound
0302 clinical medicine
Alzheimer Disease
Neoplasms
Autophagy
Genetics
Ferroptosis
Humans
Medicine
Cysteine
lcsh:QH301-705.5
business.industry
lcsh:R
Parkinson Disease
Lipid Metabolism
Chemical biology
Deferoxamine
030104 developmental biology
lcsh:Biology (General)
chemistry
Cancer research
Lipid Peroxidation
medicine.symptom
Reactive Oxygen Species
business
Deferiprone
030217 neurology & neurosurgery
medicine.drug
Subjects
Details
- ISSN :
- 20593635
- Volume :
- 6
- Database :
- OpenAIRE
- Journal :
- Signal Transduction and Targeted Therapy
- Accession number :
- edsair.doi.dedup.....25366623b637ece78115b5e529a8e11d
- Full Text :
- https://doi.org/10.1038/s41392-020-00428-9