ArticleNature communications2021
Selenoprotein W ensures physiological bone remodeling by preventing hyperactivity of osteoclasts.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 79 citations in OpenAlex.
- Signal-driven interplay between lipid peroxidation and ferroptosis orchestrates osteoarthritis degeneration.Journal of orthopaedic translation · 2026Review
- Current Advances in the Physiological Roles of the Thioredoxin-Like Family of Selenoproteins.Biological trace element research · 2026Review
- Plant-based macronutrients and micronutrients in combating osteoporosis: research insights and molecular pathways.RSC advances · 2026Review
- Article
- Metabolic Functions and Mechanisms of Selenium, Selenocysteine, and GPX4 Mediated Immune Regulation Through Autophagy in Solid Tumors.Food science & nutrition · 2025Review
- Advancement in smart bone implants: the latest multifunctional strategies and synergistic mechanisms for tissue repair and regeneration.Bioactive materials · 2025Review
- Exploring the Antioxidant Roles of Cysteine and Selenocysteine in Cellular Aging and Redox Regulation.Biomolecules · 2025Review
- Selenium and selenoproteins: key regulators of ferroptosis and therapeutic targets in cancer.Journal of molecular medicine (Berlin, Germany) · 2025Review
- Translational selenium nanomedicine synergizes with nab-paclitaxel to enhance antitumor effects in esophageal squamous cell cancer via selenoprotein N-mediated ER stress.Journal of nanobiotechnology · 2025Article
- Screening of Salsola imbricata extract impacts against acrylamide induced hepatic toxicity in rats through the regulation of different global gene expression.Toxicology research · 2025Article
- Telomere Length as Both Cause and Consequence in Type 1 Diabetes: Evidence from Bidirectional Mendelian Randomization.Biomedicines · 2025Article
- The spinal consequences of HT-2 toxin and selenium deficiency during bone maturation in mice.Mycotoxin research · 2025Article
- Denosumab ameliorates osteoarthritis by protecting cartilage against degradation and modulating subchondral bone remodeling.Regenerative therapy · 2024Article
- Selenium nanoparticles ameliorate lumbar disc degeneration by restoring GPX1-mediated redox homeostasis and mitochondrial function of nucleus pulposus cells.Journal of nanobiotechnology · 2024Article
- Versatility of 14-3-3 proteins and their roles in bone and joint-related diseases.Bone research · 2024Review
- Erythropoietin regulates osteoclast formation via up-regulating PPARγ expression.Molecular medicine (Cambridge, Mass.) · 2024Article
- Kurarinone, a flavonoid from Radix Sophorae Flavescentis, inhibits RANKL-induced osteoclastogenesis in mouse bone marrow-derived monocyte/macrophages.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- A Se Nanoparticle/MgFe-LDH Composite Nanosheet as a Multifunctional Platform for Osteosarcoma Eradication, Antibacterial and Bone Reconstruction.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Nutrition and Bone Marrow Adiposity in Relation to Bone Health.Physiological research · 2024Review
- Unveiling Genetic Potential for Equine Meat Production: A Bioinformatics Approach.Animals : an open access journal from MDPI · 2024Article
Corrections and comments
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Authors and funding
16 authors at 8 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Selenoproteins containing selenium in the form of selenocysteine are critical for bone remodeling. However, their underlying mechanism of action is not fully understood. Herein, we report the identification of selenoprotein W (SELENOW) through large-scale mRNA profiling of receptor activator of nuclear factor (NF)-κΒ ligand (RANKL)-induced osteoclast differentiation, as a protein that is downregulated via RANKL/RANK/tumour necrosis factor receptor-associated factor 6/p38 signaling. RNA-sequencing analysis revealed that SELENOW regulates osteoclastogenic genes. SELENOW overexpression enhances osteoclastogenesis in vitro via nuclear translocation of NF-κB and nuclear factor of activated T-cells cytoplasmic 1 mediated by 14-3-3γ, whereas its deficiency suppresses osteoclast formation. SELENOW-deficient and SELENOW-overexpressing mice exhibit high bone mass phenotype and osteoporosis, respectively. Ectopic SELENOW expression stimulates cell-cell fusion critical for osteoclast maturation as well as bone resorption. Thus, RANKL-dependent repression of SELENOW regulates osteoclast differentiation and blocks osteoporosis caused by overactive osteoclasts. These findings demonstrate a biological link between selenium and bone metabolism.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.