ArticleNature communications2025
Regulation of senescence-associated secretory phenotypes in osteoarthritis by cytosolic UDP-GlcNAc retention and O-GlcNAcylation.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed.
- Integrative Proteome-Wide Mendelian Randomization and Multi-Omics Analysis Identify ADM and CFH as Candidate Genes for Osteoarthritis.Biomedicines · 2026Article
- TGFBI Maintains Fibrocartilage Homeostasis by Restraining O-GlcNAcylation to Inactivate and Destabilize ADAMTS16 in Temporomandibular Joint Osteoarthritis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- OGT regulates histone demethylation and alleviates osteoarthritis progression by O-GlcNAcylation of KDM6B.Journal of advanced research · 2026Article
- Cross-talk between glycosylation pathways: Mechanistic insights and implications for human diseases.Molecular metabolism · 2026Review
- Characterization of pain-related mechanisms and bone destruction in mild and severe monoiodoacetate-induced hip arthropathy in rats.BMC musculoskeletal disorders · 2026Article
- GATA4-Driven Transcription of HtrA1 Promotes Cellular Senescence in Ménière's Disease and Age-Related Audio-Vestibular Dysfunction.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Distinct O-Linked Glycosylation Systems in Signaling and Immune Regulation.International journal of molecular sciences · 2026Review
- Anti-Photoaging Activity of a Structurally Optimized Curcumin Analogue (THHGV-5) in UV-B-Irradiated Human Dermal Fibroblasts: An Integrated In Silico and In Vitro Study.Cell biochemistry and biophysics · 2026Article
- Site-specific glycosylation of Sec24D and myoferlin recruit ERGIC to ER exit sites for collagen trafficking.Nature communications · 2026Article
- Towards a context-aware framework for cellular senescence.Biogerontology · 2026Review
- Cuttlefish ink nanoparticle hydrogels ameliorate osteoarthritis via concurrent inhibition of macrophage pyroptosis and chondrocyte senescence.Journal of nanobiotechnology · 2026Article
- O-GlcNAcylation regulates PPAR-driven metabolic programming in intestinal stem cells.bioRxiv : the preprint server for biology · 2026Article
- Time-resolved multiomics profiling reveals chromatin O-GlcNAc modification promotes senescence-associated transcriptional program.Nature communications · 2026Article
- O-GlcNAcylation in novel regulated cell death: ferroptosis, pyroptosis, and necroptosis.Cell death discovery · 2025Review
- Genomic structural equation modeling decodes skeletal aging: novel loci discovery and multisystem genetic crosstalk.Journal of translational medicine · 2025Article
- Targeting the senescence-associated secretory phenotype to modify osteoarthritis in aging.Inflammopharmacology · 2025Review
- Cytosolic phospholipase A2 as a therapeutic target for degenerative joint diseases.Bone research · 2025Article
- O-GlcNAcylation of nuclear proteins in the mouse liver exhibit daily oscillations that are influenced by meal timing.PLoS biology · 2025Article
- Biomarkers of aging as it relates osteoarthritis: we can't improve what we can't measure.Connective tissue research · 2025Review
- Functional Burden and Quality of Life in Hip and Knee Osteoarthritis: A Cross-Sectional Study.Medicina (Kaunas, Lithuania) · 2025Article
Corrections and comments
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Authors and funding
19 authors.
Funding
Abstract
UDP-GlcNAc serves as a building block for glycosaminoglycan (GAG) chains in cartilage proteoglycans and simultaneously acts as a substrate for O-GlcNAcylation. Here, we show that transporters for UDP-GlcNAc to the endoplasmic reticulum (ER) and Golgi are significantly downregulated in osteoarthritic cartilage, leading to increased cytosolic UDP-GlcNAc and O-GlcNAcylation in chondrocytes. Mechanistically, upregulated O-GlcNAcylation governs the senescence-associated secretory phenotype (SASP) by stabilizing GATA4 via O-GlcNAcylation at S406, which compromises its degradation by p62-mediated selective autophagy. Elevated O-GlcNAcylation in the superficial layer of osteoarthritic cartilage coincides with increased GATA4 levels. The topical deletion of Gata4 in this cartilage layer ameliorates post-traumatic osteoarthritis (OA) in mice while inhibiting O-GlcNAc transferase mitigates OA by decreasing GATA4 levels. Excessive glucosamine-induced O-GlcNAcylation stabilizes GATA4 in chondrocytes and exacerbates post-traumatic OA in mice. Our findings elucidate the role of UDP-GlcNAc compartmentalization in regulating secretory pathways associated with chronic joint inflammation, providing a senostatic strategy for the treatment of OA.
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Registered trials
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