Regulatory mechanism of ferroptosis, a new mode of cell death

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