Fibroblast-Myofibroblast Transition in Osteoarthritis Progression: Current Insights.
Ruixin Peng1, Qiyuan Lin1, Zhen Yang1
1Arthritis Clinical and Research Center, Peking University People's Hospital, No. 11 Xizhimen South Street, Beijing 100044, China.
Osteoarthritis progression is driven by synovial fibrosis, where fibroblast-like synoviocytes transition into myofibroblasts. Targeting this fibroblast-myofibroblast transition (FMT) offers new therapeutic strategies for joint disease.
Area of Science:
- Rheumatology and Molecular Biology
- Cellular and Tissue Engineering
Background:
- Osteoarthritis (OA) is characterized by cartilage degradation and synovial fibrosis.
- Synovial fibrosis involves fibroblast-like synoviocytes (FLSs) transitioning to myofibroblasts, depositing excess extracellular matrix (ECM).
- This process stiffens the joint capsule, exacerbating inflammation, cartilage damage, and dysfunction.
Purpose of the Study:
- To review the role of fibroblast-myofibroblast transition (FMT) in OA pathogenesis.
- To examine molecular pathways driving OA-related FMT.
- To discuss therapeutic strategies targeting synovial fibrosis in OA.
Main Methods:
- Systematic review of literature on synovial fibrosis and FMT in OA.
- Analysis of molecular pathways including TGF-β, Wnt/β-catenin, YAP/TAZ, and inflammation.
- Evaluation of emerging therapeutic targets for OA.
Main Results:
- FLS to myofibroblast transition (FMT) is a key driver of OA pathology.
- Specific molecular pathways (TGF-β, Wnt/β-catenin, YAP/TAZ) mediate OA-related FMT.
- Synovial fibrosis significantly contributes to OA severity and joint dysfunction.
Conclusions:
- The fibroblast-myofibroblast axis is central to OA progression.
- Targeting synovial fibrosis and FMT presents a promising therapeutic avenue for OA.
- Further research is needed to fully elucidate and exploit these mechanisms for clinical benefit.
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