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Distinct subsets of synovial fibroblasts control cartilage destruction in joint diseases

1, 2, 3, 4, 5


  1. Department of Emergency Medicine, Far Eastern Memorial Hospital, New Taipei City, Taiwan.
  2. Department of Orthopaedics, Chu Shang Show Chwan Hospital, Nantou County, Taiwan.
  3. Department of Biotechnology and Laboratory Science in Medicine, National Yang-Ming Chiao Tung University, Taipei, and Institute of Biopharmaceutical Sciences, National Yang-Ming Chiao Tung University, Taipei, Taiwan.
  4. Department of Orthopaedic Surgery, Far Eastern Memorial Hospital, New Taipei City, and Graduate School of Biotechnology and Bioengineering, Yuan Ze University, Taoyuan City, Taiwan.
  5. Department of Medical Research, Far Eastern Memorial Hospital, New Taipei City, Taiwan.


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PMID: 37706287 [PubMed]

Received: 30/05/2023
Accepted : 28/08/2023
In Press: 06/09/2023


Inflammation-induced bone destruction is the main cause of progressive joint damage in rheumatoid arthritis (RA) and osteoarthritis (OA). In addition, depending on the tissue microenvironment stimulators, the synovium transforms into a hyperplastic invasive tissue. The synovium includes two specific subsets of fibroblasts surrounding the joints: lining and sublining synovial fibroblasts (SFs). These SFs grow and interact with immune cells invading the bone and cartilage; specifically, SFs, which are the major mesenchymal cells in the joints, develop an aggressive phenotype, thereby producing cytokines and proteases involved in arthritis pathogeneses. Transcriptomic differences in the heterogeneity of SFs reflect the joint-specific origins of the SFs interacting with immune cells. To understand the subsets of SFs that lead to joint damage in arthritis, clarifying the distinct phenotypes and properties of SFs and understanding how they influence bone cells, such as osteoclasts and chondrocytes, is crucial. This review provides an overview of the advancements in the understanding of SF subsets and features, which may aid in identifying newer therapeutic targets.


Rheumatology Article