ArticleNature communications2022
Selenophosphate synthetase 1 deficiency exacerbates osteoarthritis by dysregulating redox homeostasis.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.
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Who cites it
66 citing papers in PubMed.
- Redox-Regulating Propolis- and Honey-Containing Hydrogels in Osteoarthritis.Antioxidants (Basel, Switzerland) · 2026Review
- Selenium, Selenoprotein P, and Gut Dysbiosis are Associated with Cartilage Damage in Osteoarthritis Patients.Biological trace element research · 2026Article
- The Role of Metals and Trace Elements in the Pathogenesis of Osteoarthritis and Other Rheumatic Diseases.International journal of molecular sciences · 2026Review
- Purinergic signaling in osteoarthritis: Mechanistic insights into pathogenesis and therapeutic targeting.Genes & diseases · 2026Review
- Cold Atmospheric Plasma as a Potential Disease-Modifying Therapy for Osteoarthritis.Biomedicines · 2026Review
- Targeted Intra-Articular PRGF Delivery Using Enzyme-Powered Nanobots for Chondral Lesions: A Prospective Experimental Study with Biomarker Evaluation in Rabbits (Animals : an open access journal from MDPI · 2026Article
- Network Analysis Identifies Microsomal Glutathione S-Transferase as a Potential Regulator of Oxidative Stress and Proteasome Dysfunction in Human Osteoarthritic Menisci.FASEB bioAdvances · 2026Article
- Genetics of selenoproteins and selenoprotein metabolism - An overview of current concepts and emerging aspects.Redox biology · 2026Review
- Cycloastragenol attenuates osteoarthritis by restoring chondrocyte senescence via the NRF2/NF-κB signaling axis.Scientific reports · 2026Article
- Chondrocyte Senescence in Osteoarthritis: Potential Targets and Pharmacological Interventions.Cartilage · 2026Article
- Circulating Essential Trace Element and Mineral Levels in Female Patients with Knee or Concomitant Knee and Hip Osteoarthritis.Biological trace element research · 2026Article
- Metformin Attenuates Osteoarthritis Progression by Modulating Mitochondrial Dynamics via Activation of the AMPK/Drp1 Pathway.Journal of inflammation research · 2026Article
- Remodeling of senescent macrophages in synovium alleviates trauma- and aging-induced osteoarthritis.Bioactive materials · 2026Article
- Inhibition of CDK9 alleviates osteoarthritis by suppressing inflammation and reducing chondrocyte apoptosis.Frontiers in pharmacology · 2026Article
- Pathogenesis of Osteoarthritis: Mechanisms of Action of Disulfidptosis and Targeted Therapeutic Strategies.Drug design, development and therapy · 2026Review
- Cellular senescence in musculoskeletal diseases: biological mechanisms and clinical implications.Theranostics · 2026Review
- Molecular characterization and prognostic modeling of liquid-liquid phase separation-related genes in osteosarcoma based on single-cell sequencing and weighted gene co-expression network analysis.Translational cancer research · 2025Article
- Dissecting the role of SEPHS1 in shaping an immunosuppressive microenvironment to promote tumor progression.Cancer immunology, immunotherapy : CII · 2025Article
- Exploring the Antioxidant Roles of Cysteine and Selenocysteine in Cellular Aging and Redox Regulation.Biomolecules · 2025Review
- Molten-Salt-Mediated Synthesis of Atomic Manganese/Cobalt Catalysts on Bioceramic Microparticles for Catalytic Anti-Osteoarthritis Treatments.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
6 more citing papers are in PubMed but not listed here.
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Authors and funding
12 authors.
Funding
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Abstract
Aging and mechanical overload are prominent risk factors for osteoarthritis (OA), which lead to an imbalance in redox homeostasis. The resulting state of oxidative stress drives the pathological transition of chondrocytes during OA development. However, the specific molecular pathways involved in disrupting chondrocyte redox homeostasis remain unclear. Here, we show that selenophosphate synthetase 1 (SEPHS1) expression is downregulated in human and mouse OA cartilage. SEPHS1 downregulation impairs the cellular capacity to synthesize a class of selenoproteins with oxidoreductase functions in chondrocytes, thereby elevating the level of reactive oxygen species (ROS) and facilitating chondrocyte senescence. Cartilage-specific Sephs1 knockout in adult mice causes aging-associated OA, and augments post-traumatic OA, which is rescued by supplementation of N-acetylcysteine (NAC). Selenium-deficient feeding and Sephs1 knockout have synergistic effects in exacerbating OA pathogenesis in mice. Therefore, we propose that SEPHS1 is an essential regulator of selenium metabolism and redox homeostasis, and its dysregulation governs the progression of OA.
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