Regulated cell death is a genetically programmed cell death associated with the maintenance of homeostasis and disease development.
Apoptosis, pyroptosis, and necroptosis are classical forms of regulated cell death that play important roles in various diseases.
Ferroptosis was a regulated cell death described by Dixon et al. who used elastin to treat cancer cells containing oncogene mutations.
They found an iron-dependent and lipid peroxidation-triggered cell death pathway, which relies on iron-generated reactive oxygen species.
The pathway was independent of caspase, adenosine triphosphate exhaustion, mitochondria reactive oxygen species generation, the permeability of the mitochondria outer membrane, and increased concentration of intracellular calcium ion.
This distinct form of cell death is significantly different from other forms of cell death morphologically, biochemically, genetically, and metabolically.
Three mainstream pathways have been identified in ferroptosis: glutathione peroxidase 4-glutathione (GPx-4-GSH) pathway, ferroptosis suppressor protein 1-ubiquinone-reduced nicotinamide adenine dinucleotide phosphate [FSP1-CoQ-NAD(P)H] axis, and dihydroorotate dehydrogenase (DHODH) signaling.
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