Mitochondrial Regulation of Ferroptosis in Cancer Therapy

Author:

Cheng Xiaoxia1,Zhang Jiale2,Xiao Yichen2,Wang Zhihang2,He Jin2,Ke Mengquan2,Liu Sijie2,Wang Qun1,Zhang Lei1ORCID

Affiliation:

1. School of Basic Medical Science, Henan University, Kaifeng 475004, China

2. School of Clinical Medicine, Henan University, Kaifeng 475004, China

Abstract

Ferroptosis, characterized by glutamate overload, glutathione depletion, and cysteine/cystine deprivation during iron- and oxidative-damage-dependent cell death, is a particular mode of regulated cell death. It is expected to effectively treat cancer through its tumor-suppressor function, as mitochondria are the intracellular energy factory and a binding site of reactive oxygen species production, closely related to ferroptosis. This review summarizes relevant research on the mechanisms of ferroptosis, highlights mitochondria’s role in it, and collects and classifies the inducers of ferroptosis. A deeper understanding of the relationship between ferroptosis and mitochondrial function may provide new strategies for tumor treatment and drug development based on ferroptosis.

Funder

National Natural Science Foundation of China

Key R&D and Promotion Projects in Henan Province

Key Scientific Research Projects of Colleges and Universities in Henan Province

Kaifeng Science and Technology Development Plan

Publisher

MDPI AG

Subject

Inorganic Chemistry,Organic Chemistry,Physical and Theoretical Chemistry,Computer Science Applications,Spectroscopy,Molecular Biology,General Medicine,Catalysis

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