Fibroblast-Myofibroblast Transition in Osteoarthritis Progression: Current Insights.
- Publisher:
- MDPI AG
- Publication Type:
- Journal Article
- Citation:
- International Journal of Molecular Sciences, 2025, 26, (16), pp. 1-21
- Issue Date:
- 2025-08-15
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Full metadata record
| Field | Value | Language |
|---|---|---|
| dc.contributor.author | Peng, R | |
| dc.contributor.author | Lin, Q | |
| dc.contributor.author | Yang, Z | |
| dc.contributor.author | Li, H | |
| dc.contributor.author | Li, JJ | |
| dc.contributor.author | Xing, D | |
| dc.date.accessioned | 2026-01-15T04:07:04Z | |
| dc.date.available | 2025-08-10 | |
| dc.date.available | 2026-01-15T04:07:04Z | |
| dc.date.issued | 2025-08-15 | |
| dc.identifier.citation | International Journal of Molecular Sciences, 2025, 26, (16), pp. 1-21 | |
| dc.identifier.issn | 1661-6596 | |
| dc.identifier.issn | 1422-0067 | |
| dc.identifier.uri | http://hdl.handle.net/10453/191864 | |
| dc.description.abstract | Osteoarthritis (OA) is a multifactorial joint disease traditionally characterized by cartilage degradation, while growing evidence underscores the critical role of synovial fibrosis in driving disease progression. The synovium exhibits pathological remodeling in OA, primarily due to the phenotypic transition of fibroblast-like synoviocytes (FLSs) into myofibroblasts. This fibroblast-myofibroblast transition (FMT) results in excessive deposition of extracellular matrix (ECM) and increased tissue stiffness and contractility, collectively contributing to chronic inflammation and fibrotic stiffening of the joint capsule. These fibrotic changes not only impair synovial function but also exacerbate cartilage degeneration, nociceptive sensitization, and joint dysfunction, thereby amplifying OA severity. Focusing on the frequently overlooked role of the FMT of synovial fibroblasts in OA, this review introduces the biological characteristics of FLSs and myofibroblasts and systematically examines the key molecular pathways implicated in OA-related FMT, including TGF-β, Wnt/β-catenin, YAP/TAZ, and inflammatory signaling cascades. It also discusses emerging therapeutic strategies targeting synovial fibrosis and FMT and considers their implications for the clinical management of OA. By highlighting recent advances and unresolved challenges, this review provides critical insights into the fibroblast-myofibroblast axis as a central contributor to OA progression and a promising therapeutic target for modifying disease trajectory. | |
| dc.format | Electronic | |
| dc.language | eng | |
| dc.publisher | MDPI AG | |
| dc.relation.ispartof | International Journal of Molecular Sciences | |
| dc.relation.isbasedon | 10.3390/ijms26167881 | |
| dc.rights | info:eu-repo/semantics/openAccess | |
| dc.subject | 0399 Other Chemical Sciences, 0604 Genetics, 0699 Other Biological Sciences | |
| dc.subject.classification | Chemical Physics | |
| dc.subject.classification | 3101 Biochemistry and cell biology | |
| dc.subject.classification | 3107 Microbiology | |
| dc.subject.classification | 3404 Medicinal and biomolecular chemistry | |
| dc.subject.mesh | Animals | |
| dc.subject.mesh | Disease Progression | |
| dc.subject.mesh | Extracellular Matrix | |
| dc.subject.mesh | Fibroblasts | |
| dc.subject.mesh | Humans | |
| dc.subject.mesh | Myofibroblasts | |
| dc.subject.mesh | Osteoarthritis | |
| dc.subject.mesh | Signal Transduction | |
| dc.subject.mesh | Synovial Membrane | |
| dc.subject.mesh | Synoviocytes | |
| dc.subject.mesh | Humans | |
| dc.subject.mesh | Osteoarthritis | |
| dc.subject.mesh | Myofibroblasts | |
| dc.subject.mesh | Fibroblasts | |
| dc.subject.mesh | Disease Progression | |
| dc.subject.mesh | Animals | |
| dc.subject.mesh | Synoviocytes | |
| dc.subject.mesh | Synovial Membrane | |
| dc.subject.mesh | Signal Transduction | |
| dc.subject.mesh | Extracellular Matrix | |
| dc.subject.mesh | Synovial Membrane | |
| dc.subject.mesh | Extracellular Matrix | |
| dc.subject.mesh | Fibroblasts | |
| dc.subject.mesh | Animals | |
| dc.subject.mesh | Humans | |
| dc.subject.mesh | Osteoarthritis | |
| dc.subject.mesh | Disease Progression | |
| dc.subject.mesh | Signal Transduction | |
| dc.subject.mesh | Myofibroblasts | |
| dc.subject.mesh | Synoviocytes | |
| dc.subject.mesh | Humans | |
| dc.subject.mesh | Osteoarthritis | |
| dc.subject.mesh | Myofibroblasts | |
| dc.subject.mesh | Fibroblasts | |
| dc.subject.mesh | Disease Progression | |
| dc.subject.mesh | Animals | |
| dc.subject.mesh | Synoviocytes | |
| dc.subject.mesh | Synovial Membrane | |
| dc.subject.mesh | Signal Transduction | |
| dc.subject.mesh | Extracellular Matrix | |
| dc.title | Fibroblast-Myofibroblast Transition in Osteoarthritis Progression: Current Insights. | |
| dc.type | Journal Article | |
| utslib.citation.volume | 26 | |
| utslib.location.activity | Switzerland | |
| utslib.for | 0399 Other Chemical Sciences | |
| utslib.for | 0604 Genetics | |
| utslib.for | 0699 Other Biological Sciences | |
| pubs.organisational-group | University of Technology Sydney | |
| pubs.organisational-group | University of Technology Sydney/Faculty of Engineering and Information Technology | |
| pubs.organisational-group | University of Technology Sydney/Faculty of Engineering and Information Technology/School of Biomedical Engineering | |
| pubs.organisational-group | University of Technology Sydney/UTS Groups | |
| pubs.organisational-group | University of Technology Sydney/UTS Groups/Centre for Health Technologies (CHT) | |
| utslib.copyright.status | open_access | * |
| pubs.consider-herdc | false | |
| dc.rights.license | This work is licensed under a Creative Commons Attribution 4.0 International License (CC BY 4.0). To view a copy of this license, visit https://creativecommons.org/licenses/by/4.0/ | |
| dc.date.updated | 2026-01-15T04:07:02Z | |
| pubs.issue | 16 | |
| pubs.publication-status | Published | |
| pubs.volume | 26 | |
| utslib.citation.issue | 16 |
Abstract:
Osteoarthritis (OA) is a multifactorial joint disease traditionally characterized by cartilage degradation, while growing evidence underscores the critical role of synovial fibrosis in driving disease progression. The synovium exhibits pathological remodeling in OA, primarily due to the phenotypic transition of fibroblast-like synoviocytes (FLSs) into myofibroblasts. This fibroblast-myofibroblast transition (FMT) results in excessive deposition of extracellular matrix (ECM) and increased tissue stiffness and contractility, collectively contributing to chronic inflammation and fibrotic stiffening of the joint capsule. These fibrotic changes not only impair synovial function but also exacerbate cartilage degeneration, nociceptive sensitization, and joint dysfunction, thereby amplifying OA severity. Focusing on the frequently overlooked role of the FMT of synovial fibroblasts in OA, this review introduces the biological characteristics of FLSs and myofibroblasts and systematically examines the key molecular pathways implicated in OA-related FMT, including TGF-β, Wnt/β-catenin, YAP/TAZ, and inflammatory signaling cascades. It also discusses emerging therapeutic strategies targeting synovial fibrosis and FMT and considers their implications for the clinical management of OA. By highlighting recent advances and unresolved challenges, this review provides critical insights into the fibroblast-myofibroblast axis as a central contributor to OA progression and a promising therapeutic target for modifying disease trajectory.
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