ArticleRedox biology2025
The selenoprotein P/ApoER2 axis facilitates selenium accumulation in selenoprotein P-accepting cells and confers prolonged resistance to ferroptosis.
Article in Redox biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Pediococcus acidilactici ZQ-19 Ameliorates Ulcerative Colitis via Remodeling Gut Microbiota and Glutathione Redox Homeostasis.Probiotics and antimicrobial proteins · 2026Article
- Promotion of Lead-induced Cytotoxicity in Differentiating Neural Cells and Protective Effects of Selenium.Biological trace element research · 2026Article
- Genetics of selenoproteins and selenoprotein metabolism - An overview of current concepts and emerging aspects.Redox biology · 2026Review
- Selenium and selenoproteins in age-related metabolic diseases: mechanistic insights and translational perspectives.Frontiers in nutrition · 2026Review
- Selenium-Enriched Microorganisms: Metabolism, Production, and Applications.Microorganisms · 2025Review
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Authors and funding
10 authors.
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Abstract
The essential trace element selenium (Se) plays a significant role in redox homeostasis, while Se is very reactive and has a potent toxicity. Understanding the molecular machinery that supports Se metabolism is important for the both physiological and pathophysiological context. Incorporated Se is translated/transformed in the liver into selenoprotein P (SeP; encoded by Selenop), an extracellular Se carrier protein that effectively transports Se to the cells via the binding to its receptor apolipoprotein E receptor 2 (ApoER2), which is taken up by cells. The present study shows that SeP is a source of Se that accumulates intracellularly and can be utilized for prolonged periods under Se-deficient conditions. In cultured cells (RD and SH-SY5Y), glutathione peroxidase (GPX) expression induced by Se supply via the SeP/ApoER2 pathway was maintained longer during Se deficiency than inorganic Se, which was promoted by ApoER2 overexpression. SeP-deficient mice showed a faster decline in brain Se levels when fed a Se-deficient diet. Preserved GPX expression induced by this SeP/ApoER2 axis contributed to oxidative stress and ferroptosis resistance, suggesting that this redundant Se metabolism contributes to prolonged Se utilization and cytoprotection.
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