ArticleBone research2025
Synovial fibroblast derived small extracellular vesicles miRNA15-29148 promotes articular chondrocyte apoptosis in rheumatoid arthritis.
Article in Bone research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed.
- FGFR1 signaling in rheumatoid arthritis: Mechanisms of bone destruction and therapeutic targeting (Review).International journal of molecular medicine · 2026Review
- Targeting FOSL1-KCa3.1 inhibits ferroptosis and cartilage destruction by suppressing mitochondrial hyperfusion.Acta pharmacologica Sinica · 2026Article
- Therapeutic Extracellular Vesicles from Synovial Fibroblast-Primed MSCs for Osteoarthritis Treatment.Advanced healthcare materials · 2026Article
- Comment: Comparative Evaluation of Single and Combination Pharmacologic and Device-Based Anti-scar Therapies in a Murine Linear Wound Model.Aesthetic plastic surgery · 2026Article
- Apoptotic bodies in bone homeostasis and skeletal disease: biology and therapeutic implications.Apoptosis : an international journal on programmed cell death · 2026Review
- Transcriptome Analysis of Differentially Expressed Genes and Molecular Pathways Involved During Osteoclast Differentiation.Molecular biotechnology · 2026Article
- Cancer Gene Therapy Utilizing NF-κB-regulated Expression of a miRNA Targeting RelA.Applied biochemistry and biotechnology · 2026Article
- Targeting the gut‑bone axis through exercise: A novel approach to osteoporosis prevention and treatment (Review).International journal of molecular medicine · 2026Review
- Convallatoxin ameliorates fibroblast-like synoviocytes-mediated synovial inflammation and joint destruction in rheumatoid arthritis by targeting IDH1.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Syndecan-2 Regulates Integrin-β1 to Influence the Abnormal Subchondral Bone in Early-stage Knee Osteoarthritis.Applied biochemistry and biotechnology · 2026Article
- Comment: Insights into the Management of Trapdoor Deformity After Facial Skin Flap Reconstruction.Aesthetic plastic surgery · 2026Article
- Cell-free therapeutics for non-healing wounds: role of MSC-derived exosomes in macrophage polarization, angiogenesis, and fibroblast-mediated ECM remodeling-bridging preclinical insights to clinical translation.Inflammopharmacology · 2026Review
- Article
- Extracellular vesicle-mediated immune crosstalk in rheumatoid arthritis synovium: mechanistic insights and translational challenges.Frontiers in immunology · 2026Review
- Systemic regulation of rheumatoid arthritis by mesenchymal stem cells: from immune homeostasis to microbiota modulation.Frontiers in immunology · 2026Review
- Extracellular vesicles in rheumatoid arthritis: emerging roles in progression, diagnosis, and therapeutic development.Frontiers in immunology · 2026Review
- The PANoptotic mosaic of rheumatoid arthritis: epitranscriptomic regulation, systemic relays, and precision death-mode editing.Frontiers in immunology · 2026Review
- Engineering the Future: Strategic Advances in Extracellular Vesicle-Mediated Drug Delivery Systems.International journal of nanomedicine · 2026Review
- METTL3 promotes chondrocyte injury in osteoarthritis by increasing CTSB expression.Journal of orthopaedic surgery and research · 2025Article
- AP39 suppresses osteoclast differentiation and neural factor expression under inflammatory condition.Journal of orthopaedic surgery and research · 2025Article
Corrections and comments
- Erratum issued
Authors and funding
15 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rheumatoid arthritis (RA) is a systemic autoimmune disease in which synovial fibroblasts (SFs) maintain chronic inflammation by secreting proinflammatory mediators, leading to joint destruction. While the role of proinflammatory mediators in this process is well-established, the contribution of non-inflammatory regulators in SFs to joint pathology remains poorly understood. In this study, we investigated the non-inflammatory role of SFs in RA using a co-culture model, and found that SFs from RA patients promote apoptosis of human chondrocytes. Mechanistic investigations reveal that SFs can secrete small extracellular vesicles (sEVs), which are taken up by chondrocytes and induce chondrocyte apoptosis in both normal chondrocytes and chondrocytes from patients with RA. sEV-derived miRNA 15-29148 are identified as key signaling molecules mediating the apoptosis effects of chondrocytes. Further studies reveal that SF-derived miRNA 15-29148 targeting CIAPIN1 results in increased chondrocyte apoptosis. We further demonstrate that SF-derived miRNA 15-29148 is transferred to chondrocytes, exacerbating cartilage damage in vivo. Moreover, chondrocyte-specific aptamer-modified polyamidoamine nanoparticles not only ameliorated RA but also prevented its onset. This study suggests that, in RA, the secretion of specific sEV-miRNAs from SFs plays a crucial role in promoting chondrocyte apoptosis, potentially through non-inflammatory regulation, and that sEV-miRNA inhibition in SFs may represent an early preventive treatment strategy for cartilage degradation in RA.
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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 Socratic graph.