ArticleNature communications2025
ER O-glycosylation in synovial fibroblasts drives cartilage degradation.
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 9 papers.
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Who cites it
9 citing papers in PubMed.
- An intelligent tribological hydrogel delivering 9,10-DiOH activates cuproptosis for comprehensive rheumatoid arthritis intervention.Materials today. Bio · 2026Article
- Multi-Technique Integration Identifies O-GlcNAc Transferase in Fibroblast-Like Synoviocytes as a Therapeutic Target for Rheumatoid Arthritis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- ROS-responsive injectable hydrogel enables controlled release of human adipose tissue-derived extracellular vesicles for multifaceted osteoarthritis therapy.Journal of nanobiotechnology · 2026Article
- GALNT1 drives aggressive phenotypes of rheumatoid synoviocytes via NEK9 O-glycosylation.JCI insight · 2026Article
- Distinct O-Linked Glycosylation Systems in Signaling and Immune Regulation.International journal of molecular sciences · 2026Review
- Research progress in the role and mechanism of GALNT3 in human diseases (Review).Biomedical reports · 2026Review
- Low-input deep learning platform for citrullinated peptide identification, autoantigen discovery and rheumatoid arthritis treatment stratification.Nature biomedical engineering · 2026Article
- Glycosylation switch in synovial fibroblasts promotes ECM degradation.Nature reviews. Rheumatology · 2025Article
- ER-resident proteins are key players in cartilage and bone homeostasis.Frontiers in cell and developmental biology · 2025Review
Corrections and comments
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
How arthritic synovial fibroblasts (SFs) activate cartilage ECM degradation remains unclear. GALNT enzymes initiate O-glycosylation in the Golgi; when relocated to the ER, their activity stimulates ECM degradation. Here, we show that in human rheumatoid and osteoarthritic synovial SFs, GALNTs are relocated to the ER. In an RA mouse model, GALNTs relocation occurs shortly before arthritis symptoms and abates as the animal recovers. An ER GALNTs inhibitor prevents cartilage ECM degradation in vitro and expression of this chimeric protein in SFs results in the protection of cartilage. One of the ER targets of GALNTs is the resident protein Calnexin, which is exported to the cell surface of arthritic SFs. Calnexin participates in matrix degradation by reducing ECM disulfide bonds. Anti-Calnexin antibodies block ECM degradation and protect animals from RA. In sum, ER O-glycosylation is a key switch in arthritic SFs and glycosylated surface Calnexin could be a therapeutic target.
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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.