ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2024
SELENOI Functions as a Key Modulator of Ferroptosis Pathway in Colitis and Colorectal Cancer.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed.
- Selenoproteins: Minute yet vital players governing cellular fate.Genes & diseases · 2026Review
- Article
- The Interaction Between Iron and Selenium Affects Ferroptosis in Colorectal Cancer.International journal of molecular sciences · 2026Review
- Lactate Metabolism-Immune Regulation-Related Gene Signature in Lower-Grade Gliomas: Prognostic Model Development and Immune Characterization.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Towards Precision and Balance in Selenium Nutrition: From Innovation to Application.Nutrients · 2026Article
- Ferroptosis in Myocardial Fibrosis: Mechanisms and Therapeutic Insights.Antioxidants (Basel, Switzerland) · 2026Review
- From biosynthesis to function: the roles of ether lipids in cancer development and treatment.Lipids in health and disease · 2025Review
- Metabolic Functions and Mechanisms of Selenium, Selenocysteine, and GPX4 Mediated Immune Regulation Through Autophagy in Solid Tumors.Food science & nutrition · 2025Review
- Dietary Selenium-Enriched Aquatic Products for Human Health.Nutrients · 2025Review
- Targeted delivery of the GPX4 activator via HUCMSC-derived exosomes inhibits ferroptosis in spinal cord injury.Journal of nanobiotechnology · 2025Article
- Activation of the De Novo Serine Synthesis Pathway and Disruption of Insulin Signaling Induced by Supplemental SeMet in Vitro.Biological trace element research · 2025Article
- Crosstalk Between Microbiome and Ferroptosis in Diseases: From Mechanism to Therapy.Comprehensive Physiology · 2025Review
- Review
- Sulfide Quinone Oxidoreductase Alleviates Acute Ulcerative Colitis by Regulating Mitochondrial Dysfunction.MedComm · 2025Article
- Selenium and Selenoproteins: Mechanisms, Health Functions, and Emerging Applications.Molecules (Basel, Switzerland) · 2025Review
- The Inhibitory Effects of NCT503 and Exogenous Serine on High-Selenium Induced Insulin Resistance in Mice.Nutrients · 2025Article
- Redefining cell death: ferroptosis as a game-changer in ophthalmology.Frontiers in immunology · 2025Review
- Comprehensive Analysis of Selenium Metabolism and Selenoproteins-Associated Gene Signatures in Ulcerative Colitis.Journal of inflammation research · 2025Article
- Amelioration of LPS-Induced Jejunum Injury and Mucus Barrier Damage in Mice by IgY Embedded in W/O/W Emulsion.Foods (Basel, Switzerland) · 2024Article
- Ferroptosis in ischemic stroke: Animal models and mechanisms.Zoological research · 2024Review
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Authors and funding
10 authors.
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Abstract
Ferroptosis plays important roles both in normal physiology and multiple human diseases. It is well known that selenoprotein named glutathione peroxidase 4 (GPX4) is a crucial regulator for ferroptosis. However, it remains unknown whether other selenoproteins responsible for the regulation of ferroptosis, particularly in gut diseases. In this study, it is observed that Selenoprotein I (Selenoi) prevents ferroptosis by maintaining ether lipids homeostasis. Specific deletion of Selenoi in intestinal epithelial cells induced the occurrence of ferroptosis, leading to impaired intestinal regeneration and compromised colonic tumor growth. Mechanistically, Selenoi deficiency causes a remarkable decrease in ether-linked phosphatidylethanolamine (ePE) and a marked increase in ether-linked phosphatidylcholine (ePC). The imbalance of ePE and ePC results in the upregulation of phospholipase A2, group IIA (Pla2g2a) and group V (Pla2g5), as well as arachidonate-15-lipoxygenase (Alox15), which give rise to excessive lipid peroxidation. Knockdown of PLA2G2A, PLA2G5, or ALOX15 can reverse the ferroptosis phenotypes, suggesting that they are downstream effectors of SELENOI. Strikingly, GPX4 overexpression cannot rescue the ferroptosis phenotypes of SELENOI-knockdown cells, while SELENOI overexpression can partially rescue GPX4-knockdown-induced ferroptosis. It suggests that SELENOI prevents ferroptosis independent of GPX4. Taken together, these findings strongly support the notion that SELENOI functions as a novel suppressor of ferroptosis during colitis and colon tumorigenesis.
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