期刊
CELL CHEMICAL BIOLOGY
卷 27, 期 4, 页码 409-419出版社
CELL PRESS
DOI: 10.1016/j.chembiol.2020.03.012
关键词
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资金
- Deutsche Forschungsgemeinschaft (DFG) [CO 291/5-2, CO 291/7-1, PR 1752/3-1]
- German Federal Ministry of Education and Research (BMBF) through the Joint Project Modeling ALS Disease In Vitro (MAIV) [01EK1611B]
- VIP+ program NEURO-PROTEKT [03VP04260]
- Government of the Russian Federation [2019-220-07-7053]
- m4 Award by Bavarian Ministry of Economic Affairs, Regional Development and Energy (StMWi)
The trace elements iron and selenium play decisive roles in a distinct form of necrotic cell death, known as ferroptosis. While iron promotes ferroptosis by contributing to Fenton-type reactions and uncontrolled lipid autoxidation, the hallmark of ferroptosis, selenium in the form of glutathione peroxidase 4 (GPX4), subdues phospholipid peroxidation and associated cell death. Beyond the canonical cystine/glutamate antiporter system x(c)(-)/glutathione/GPX4 nexus, recent studies unveiled the second mainstay in ferroptosis entailing extra-mitechondriai ubiquinone, ferroptosis suppressor protein 1, and NAD(P)H as electron donor. Unlike GPX4, this selenium- and thiol-independent system acts on the level of peroxyl radicals in membranes thereby restraining Hold peroxidation. Therefore, ferroptosis is a multifaceted cell-death paradigm characterized by several metabolic networks, whereby metabolic dyshomeostasis may cause ferroplotic cell death and organ failure. Here, we discuss the basic features of ferroptosis with a focus on selenium, offering exciting opportunities to control diseases linked to ferroptosis, including transient ischemia reperfusion and neurodegeneration.
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