Rheumatoid arthritis (RA) is a chronic systemic autoimmune disease that mainly affects synovial joints. During the course of RA, the synovium transforms into hyperplastic invasive tissue, leading to cartilage and bone destruction. Fibroblast-like synoviocytes (FLS) in the synovial lining develop aggressive phenotypes and produce pathogenic mediators that lead to the occurrence and progression of disease, playing a major role in RA pathophysiology. Therefore, research on FLS has become the main focus within the RA field. With technical advances and the development of multi-omics comprehensive analysis approaches, it has become possible to identify different FLS subsets via high-throughput sequencing and investigate differences between FLS phenotypes, allowing for the detailed study of RA pathogenesis. This review summarizes recent works on FLS subtypes and the surface marker proteins identified for different subtypes, providing a theoretical basis and reference for future studies on FLS in RA. The current work also addresses the clinical potential of FLS surface markers in RA based on related research from other fields.

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