Abstract Coenzyme Q 10 (CoQ 10 ) is a highly conserved lipophilic redox cofactor that mediates electron transport in mitochondria and protects cells against oxidative stress. Increasing evidence has revealed that CoQ 10 and its associated oxidoreductases serve as critical regulators of ferroptosis—an iron-dependent, lipid peroxidation-driven form of cell death. Here we provide an updated overview of the canonical CoQ 10 biosynthetic pathway and the established functions of key CoQ 10 oxidoreductases. We highlight emerging insights into ferroptosis-suppressive roles of enzymes such as FSP1, DHODH and SQOR, which act by regenerating ubiquinol (CoQ 10 H 2 , reduced). In addition, we discuss newly identified CoQ 10 -related enzymes and their mechanistic contributions to ferroptosis regulation. By integrating perspectives from biochemistry, metabolism and cancer biology, this review positions CoQ 10 oxidoreductases as promising targets for ferroptosis-based cancer therapies.
Lee et al. (Wed,) studied this question.