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细胞代谢和铁死亡调节中的混杂酶SQOR

Promiscuous enzyme SQOR in cellular metabolism and ferroptosis regulation.

作者信息

Lee Jumi, Yoo Inhwan, Ahn Ihyeon, Lee Namgyu

机构信息

Department of Biomedical Science & Systems Biology, Dankook University, Cheonan 31116, Korea.

Department of Microbiology and Biotechnology, Dankook University, Cheonan 31116, Korea.

出版信息

BMB Rep. 2025 Jun;58(6):233-237.

PMID:40495478
Abstract

Ferroptosis, an iron-dependent form of programmed cell death, is primarily driven by the accumulation of lipid peroxides through radical generation, notably via the Fenton reaction. Emerging evidence highlights the intricate link between ferroptosis and cellular metabolism, with metabolic enzymes playing pivotal roles 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 a novel function in ferroptosis regulation. This review explores SQOR's canonical function in H2S metabolism and its emerging role in ferroptosis resistance through the production of ubiquinol and hydropersulfides, radical-trapping antioxidants. Additionally, we provide insights into potential future research directions, emphasizing SQOR's therapeutic relevance in ferroptosis-associated diseases. [BMB Reports 2025; 58(6): 233-237].

摘要

铁死亡是一种铁依赖性的程序性细胞死亡形式,主要由脂质过氧化物通过自由基生成而积累所驱动,特别是通过芬顿反应。新出现的证据凸显了铁死亡与细胞代谢之间的复杂联系,代谢酶在其调控中发挥着关键作用。硫化物醌氧化还原酶(SQOR),传统上因其在硫化氢(H2S)解毒和电子传递链(ETC)激活中的作用而被认可,最近被鉴定为一种具有铁死亡调控新功能的混杂酶。本综述探讨了SQOR在H2S代谢中的经典功能,以及它通过生成泛醇和氢过硫化物(自由基捕获抗氧化剂)在抗铁死亡方面的新作用。此外,我们还对未来潜在的研究方向提供了见解,强调了SQOR在铁死亡相关疾病中的治疗相关性。[《BMB报告》2025年;58(6): 233 - 237]

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本文引用的文献

1
Non-thermal atmospheric pressure plasma-irradiated cysteine protects cardiac ischemia/reperfusion injury by preserving supersulfides.非热大气压等离子体照射的半胱氨酸通过保留超硫化物来保护心脏缺血/再灌注损伤。
Redox Biol. 2025 Feb;79:103445. doi: 10.1016/j.redox.2024.103445. Epub 2024 Nov 28.
2
Nα-terminal acetylation meets ferroptosis via N-degron pathway.N端乙酰化通过N-端规则途径参与铁死亡。
Mol Cells. 2024 Dec;47(12):100160. doi: 10.1016/j.mocell.2024.100160. Epub 2024 Nov 20.
3
Exclusion of sulfide:quinone oxidoreductase from mitochondria causes Leigh-like disease in mice by impairing sulfide metabolism.
线粒体中排除硫化物:醌氧化还原酶通过损害硫化物代谢在小鼠中引发类利氏病。
J Clin Invest. 2024 Jun 13;134(15):e170994. doi: 10.1172/JCI170994.
4
Malate dehydrogenase (MDH) in cancer: a promiscuous enzyme, a redox regulator, and a metabolic co-conspirator.苹果酸脱氢酶(MDH)与癌症:多功能酶、氧化还原调节剂和代谢共谋者。
Essays Biochem. 2024 Oct 3;68(2):135-146. doi: 10.1042/EBC20230088.
5
A targetable PRR11-DHODH axis drives ferroptosis- and temozolomide-resistance in glioblastoma.靶向 PRR11-DHODH 轴可驱动脑胶质母细胞瘤中的铁死亡和替莫唑胺耐药。
Redox Biol. 2024 Jul;73:103220. doi: 10.1016/j.redox.2024.103220. Epub 2024 May 30.
6
Selenium reduction of ubiquinone via SQOR suppresses ferroptosis.硒通过 SQOR 将泛醌还原从而抑制铁死亡。
Nat Metab. 2024 Feb;6(2):343-358. doi: 10.1038/s42255-024-00974-4. Epub 2024 Feb 13.
7
Sulfide:quinone oxidoreductase alleviates ferroptosis in acute kidney injury via ameliorating mitochondrial dysfunction of renal tubular epithelial cells.硫化物:醌氧化还原酶通过改善肾小管上皮细胞线粒体功能障碍缓解急性肾损伤中的铁死亡。
Redox Biol. 2024 Feb;69:102973. doi: 10.1016/j.redox.2023.102973. Epub 2023 Nov 29.
8
Menaquinone-4 attenuates ferroptosis by upregulating DHODH through activation of SIRT1 after subarachnoid hemorrhage.甲萘醌-4 通过激活 SIRT1 上调 DHODH 减轻蛛网膜下腔出血后的铁死亡。
Free Radic Biol Med. 2024 Jan;210:416-429. doi: 10.1016/j.freeradbiomed.2023.11.031. Epub 2023 Nov 30.
9
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