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Yeungnam Univ J Med > Volume 34(2); 2017 > Article
Yeungnam University Journal of Medicine 2017;34(2):174-181.
DOI: https://doi.org/10.12701/yujm.2017.34.2.174    Published online December 31, 2017.
Novel non-apoptotic cell death: ferroptosis
Seon Min Woo, Taeg Kyu Kwon
Department of Immunology, School of Medicine, Keimyung University, Daegu, Korea. kwontk@dsmc.or.kr
Abstract
Ferroptosis is a newly recognized type of cell death that results from iron-dependent lipid peroxidation and is different from other types of cell death, such as apoptosis, necrosis, and autophagic cell death. This type of cell death is characterized by mitochondrial shrinkage with an increased mitochondrial membrane density and outer mitochondrial membrane rupture. Ferroptosis can be induced by a loss of activity of system Xc− and the inhibition of glutathione peroxidase 4, followed by the accumulation of lipid reactive oxygen species (ROS). In addition, inactivation of the mevalonate and transsulfuration pathways is involved in the induction of ferroptosis. Moreover, nicotinamide adenine dinucleotide phosphate oxidase and p53 promote ferroptosis by increasing ROS production, while heat shock protein beta-1 and nuclear factor erythroid 2-related factor 2 inhibit ferroptosis by reducing iron uptake. This article outlines the molecular mechanisms and signaling pathways of ferroptosis regulation, and explains the roles of ferroptosis in human disease.
Key Words: Ferroptosis, Non-apoptotic cell death, Iron-dependent cell death, Reactive oxygen species
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