Promiscuous enzyme SQOR in cellular metabolism and ferroptosis regulation
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Ferroptosis, an iron-dependent form of programmed cell death,is primarily driven by the accumulation of lipid peroxides throughradical generation, notably via the Fenton reaction. Emergingevidence highlights the intricate link between ferroptosis andcellular metabolism, with metabolic enzymes playing pivotalroles in its regulation. Sulfide quinone oxidoreductase (SQOR),traditionally recognized for its role in hydrogen sulfide (H2S)detoxification and electron transport chain (ETC) activation,has recently been identified as a promiscuous enzyme with anovel function in ferroptosis regulation. This review exploresSQOR’s canonical function in H2S metabolism and its emergingrole in ferroptosis resistance through the production ofubiquinol and hydropersulfides, radical-trapping antioxidants. Additionally, we provide insights into potential future researchdirections, emphasizing SQOR’s therapeutic relevance in ferroptosis-associated diseases.
Abstract
Ferroptosis, an iron-dependent form of programmed cell death,is primarily driven by the accumulation of lipid peroxides throughradical generation, notably via the Fenton reaction. Emergingevidence highlights the intricate link between ferroptosis andcellular metabolism, with metabolic enzymes playing pivotalroles in its regulation. Sulfide quinone oxidoreductase (SQOR),traditionally recognized for its role in hydrogen sulfide (H2S)detoxification and electron transport chain (ETC) activation,has recently been identified as a promiscuous enzyme with anovel function in ferroptosis regulation. This review exploresSQOR’s canonical function in H2S metabolism and its emergingrole in ferroptosis resistance through the production ofubiquinol and hydropersulfides, radical-trapping antioxidants. Additionally, we provide insights into potential future researchdirections, emphasizing SQOR’s therapeutic relevance in ferroptosis-associated diseases.