Ferroptosis in Life: To Be or Not to Be

Authors

Ling Xu
Yu'e Liu
Xi Chen
Hua Zhong
Yi Wang

Language

English

Publication Date

3-1-2023

Journal

Biomedicine & Pharmacotherapy

DOI

10.1016/j.biopha.2023.114241

PMID

36634587

Abstract

Ferroptosis is a novel type of programmed cell death, characterized by a dysregulated iron metabolism and accumulation of lipid peroxides. It features the alteration of mitochondria and aberrant accumulation of excessive iron as well as loss of the cysteine-glutathione-GPX4 axis. Eventually, the accumulated lipid peroxides result in lethal damage to the cells. Ferroptosis is induced by the overloading of iron and the accumulation of ROS and can be inhibited by the activation of the GPX4 pathway, FS1-CoQ10 pathway, GCH1-BH4 pathway, and the DHODH pathway, it is also regulated by the oncogenes and tumor suppressors. Ferroptosis involves various physiological and pathological processes, and increasing evidence indicates that ferroptosis play a critical role in cancers and other diseases. It inhibits the proliferation of malignant cells in various types of cancers and inducing ferroptosis may become a new method of cancer treatment. Many inhibitors targeting the key factors of ferroptosis such as SLC7A11, GPX4, and iron overload have been developed. The application of ferroptosis is mainly divided into two directions, i.e. to avoid ferroptosis in healthy cells and selectively induce ferroptosis in cancers. In this review, we provide a critical analysis of the concept, and regulation pathways of ferroptosis and explored its roles in various diseases, we also summarized the compounds targeting ferroptosis, aiming to promote the speed of clinical use of ferroptosis induction in cancer treatment.

Keywords

Humans, Ferroptosis, Lipid Peroxides, Apoptosis, Iron, Neoplasms, Cell death, Ferroptosis, GPX4, SLC7A11

Published Open-Access

yes

Recommended Citation

Xu, Ling; Liu, Yu'e; Chen, Xi; et al., "Ferroptosis in Life: To Be or Not to Be" (2023). Faculty and Staff Publications. 4849.
https://digitalcommons.library.tmc.edu/baylor_docs/4849