Selenium: Tracing another essential element of ferroptotic cell death.
    
    
        
    
    
        
        Cell Chem. Bio. 27, 409-419 (2020)
    
    
    
      
      
	
	    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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        Publication type
        Article: Journal article
    
 
    
        Document type
        Review
    
 
    
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        Keywords
        Ferroptosis ; Ferroptosis Suppressor Protein 1 ; Glutathione Peroxidase 4 ; Pufa ; Selenium; Glutathione-peroxidase 4; Active Organoselenium Compound; Selenoprotein-p; Vitamin-e; Lipid-peroxidation; Cancer Prevention; Thioredoxin Reductase; Selenocysteine Insertion; Targeted Disruption; Prostate-cancer
    
 
    
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        Language
        english
    
 
    
        Publication Year
        2020
    
 
    
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        HGF-reported in Year
        2020
    
 
    
    
        ISSN (print) / ISBN
        2451-9448
    
 
    
        e-ISSN
        2451-9456
    
 
    
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	    Volume: 27,  
	    Issue: 4,  
	    Pages: 409-419 
	    Article Number: ,  
	    Supplement: ,  
	
    
 
    
        
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            Publisher
            Cell Press
        
 
        
            Publishing Place
            Cambridge, Massachusetts
        
 
	
        
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        Reviewing status
        Peer reviewed
    
 
     
    
        POF-Topic(s)
        30203 - Molecular Targets and Therapies
    
 
    
        Research field(s)
        Genetics and Epidemiology
    
 
    
        PSP Element(s)
        G-506900-001
    
 
    
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        Erfassungsdatum
        2020-05-08