ArticleJCI insight2023
Glutathione limits RUNX2 oxidation and degradation to regulate bone formation.
Article in JCI insight, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
34 citing papers in PubMed, 50 citations in OpenAlex.
- Chondrocytes in fracture healing: A review of chondrocyte journey.Chinese medical journal · 2026Review
- Age-related GSS promoter methylation in BMSCs drives osteoporosis and the reversal by targeted GSH delivery.Bioactive materials · 2026Article
- METTL5 deficiency impairs osteogenesis through OSER1-dependent antioxidant regulation.JCI insight · 2026Article
- Intelligence-responsive wettability switch coating on magnesium implants for treating osteoporotic fracture.Nature communications · 2026Article
- Integrated Network Pharmacology and Proteomics Reveal That Erxian Decoction Counteracts Postmenopausal Osteoporosis via GSTA1-Mediated Oxidative Stress Suppression.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Targeting amino acid metabolic pathways: a novel therapeutic strategy for hyperuricemia-associated complications.Amino acids · 2026Review
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- Polycaprolactone scaffolds promote a regeneration-supportive metabolic response attenuated in diabetes.Regenerative biomaterials · 2026Article
- Oxidative stress and bone marrow adipocytes: Molecular mechanisms and possible implications.Journal of orthopaedic translation · 2026Review
- Melatonin Supplementation Relieves Fluoride-Induced Bone Injury via Ion Homeostasis Disorder and PINK1/Parkin-Mediated Mitophagy.Foods (Basel, Switzerland) · 2025Article
- Metabolic signatures in osteoporotic cancellous bone: a comprehensive dual-platform metabolomic analysis.BMC musculoskeletal disorders · 2025Article
- N-acetylcarnosine attenuates age-associated declines in multi-organ systems to improve survival.bioRxiv : the preprint server for biology · 2025Article
- High-fat diet, intestinal microecology and bone loss.Nutrition & metabolism · 2025Review
- Current cutting-edge omics techniques on musculoskeletal tissues and diseases.Bone research · 2025Review
- Metabolic markers detect early ostedifferentiation of mesenchymal stem cells from multiple donors.Stem cell research & therapy · 2025Article
- In vitro and in vivo study of concentrated growth factor (CGF) mediating macrophage polarization in bone defect repair.Regenerative therapy · 2025Article
- Engineering 3D-BMSC exosome-based hydrogels that collaboratively regulate bone microenvironment and promote osteogenesis for enhanced cell-free bone regeneration.Materials today. Bio · 2025Article
- Molecular crosstalk in SP7-mediated osteogenesis: Regulatory mechanisms and therapeutic potential.Osteoporosis and sarcopenia · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
Reactive oxygen species (ROS) are natural products of mitochondrial oxidative metabolism and oxidative protein folding. ROS levels must be well controlled, since elevated ROS has been shown to have deleterious effects on osteoblasts. Moreover, excessive ROS is thought to underlie many of the skeletal phenotypes associated with aging and sex steroid deficiency in mice and humans. The mechanisms by which osteoblasts regulate ROS and how ROS inhibits osteoblasts are not well understood. Here, we demonstrate that de novo glutathione (GSH) biosynthesis is essential in neutralizing ROS and establish a proosteogenic reduction and oxidation reaction (REDOX) environment. Using a multifaceted approach, we demonstrate that reducing GSH biosynthesis led to acute degradation of RUNX2, impaired osteoblast differentiation, and reduced bone formation. Conversely, reducing ROS using catalase enhanced RUNX2 stability and promoted osteoblast differentiation and bone formation when GSH biosynthesis was limited. Highlighting the therapeutic implications of these findings, in utero antioxidant therapy stabilized RUNX2 and improved bone development in the Runx2+/- haplo-insufficient mouse model of human cleidocranial dysplasia. Thus, our data establish RUNX2 as a molecular sensor of the osteoblast REDOX environment and mechanistically clarify how ROS negatively impacts osteoblast differentiation and bone formation.
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Registered trials
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.