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Novel non-apoptotic cell death: ferroptosis

새로운 non-apoptotic 세포사멸: ferroptosis

  • Woo, Seon Min (Department of Immunology, School of Medicine, Keimyung University) ;
  • Kwon, Taeg Kyu (Department of Immunology, School of Medicine, Keimyung University)
  • 우선민 (계명대학교 의과대학 면역학교실) ;
  • 권택규 (계명대학교 의과대학 면역학교실)
  • Received : 2017.10.30
  • Accepted : 2017.11.30
  • Published : 2017.12.31

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 $X_c{^-}$ 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.

Keywords

References

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