Tropical Journal of Pharmaceutical Research

Review Article | OPEN ACCESS

Regulatory mechanism of ferroptosis, a new mode of cell death

Da Liu, Guoya Li, Ang Jia, Yanyan Zhao, Chenxi Cao, Xuekun Xing

Department of Life Sciences and Technology, Xinxiang Medical University, Xinxiang, Henan 453003, PR China;

For correspondence:- Xuekun Xing Email: biyingxiao@163.com Tel:+8615637382107

Accepted: 20 October 2018 Published: 30 November 2018

Citation: Liu D, Li G, Jia A, Zhao Y, Cao C, Xing X. Regulatory mechanism of ferroptosis, a new mode of cell death. Trop J Pharm Res 2018; 17(11):2309-2316 doi: 10.4314/tjpr.v17i11.29

© 2018 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..

Abstract

Ferroptosis is a newly discovered process of cell death that differs from apoptosis, autophagy, and pyroptosis. It is closely related to tumor formation, diseases that damage tissue, and neurodegenerative diseases. Activation of the extracellular regulated protein kinase (EPK) pathway and acylCOA synthetase long-chain family member 4 (ACSL4) are indicative of ferroptosis. During ferroptosis, the mitochondrial volume becomes smaller and the double membrane density increases. The process of ferroptosis involves disruption of the material redox reaction, and changes in the levels of cystine, glutathione, NADPH, and increase of GPX4, NOX, and ROS. Iron increases significantly in ferroptosis. Divalent iron ions can greatly promote lipid oxidation, ROS accumulation, and thus promote ferroptosis. The occurrence and progress of ferroptosis are influenced by multiple factors and signaling pathways.

Keywords: Ferroptosis, Iron; Lipid, Active oxygen, Inhibitor, Inducer