Novel non-apoptotic cell death: ferroptosis
10.12701/yujm.2017.34.2.174
- Author:
Seon Min WOO
1
;
Taeg Kyu KWON
Author Information
1. Department of Immunology, School of Medicine, Keimyung University, Daegu, Korea. kwontk@dsmc.or.kr
- Publication Type:Review
- Keywords:
Ferroptosis;
Non-apoptotic cell death;
Iron-dependent cell death;
Reactive oxygen species
- MeSH:
Apoptosis;
Autophagy;
Cell Death;
Glutathione Peroxidase;
HSP27 Heat-Shock Proteins;
Humans;
Iron;
Lipid Peroxidation;
Mevalonic Acid;
Mitochondrial Membranes;
NADP;
Necrosis;
Oxidoreductases;
Reactive Oxygen Species;
Rupture
- From:Yeungnam University Journal of Medicine
2017;34(2):174-181
- CountryRepublic of Korea
- Language:Korean
-
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.
