Yeungnam Univ J Med.  2017 Dec;34(2):174-181. 10.12701/yujm.2017.34.2.174.

Novel non-apoptotic cell death: ferroptosis

• Woo SM
• Kwon TK

• KMID: 2400352
• DOI: http://doi.org/10.12701/yujm.2017.34.2.174

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.

Keyword

Ferroptosis; Non-apoptotic cell death; Iron-dependent cell death; Reactive oxygen species

MeSH Terms

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
Glutathione Peroxidase
HSP27 Heat-Shock Proteins
Iron
Mevalonic Acid
NADP
Oxidoreductases
Reactive Oxygen Species