ArticleAdvanced healthcare materials2026
Therapeutic Extracellular Vesicles from Synovial Fibroblast-Primed MSCs for Osteoarthritis Treatment.
Article in Advanced healthcare materials, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Mesenchymal stem cells (MSCs) migrate to injured tissues through a homing effect and promote tissue regeneration by secreting paracrine factors and extracellular vesicles (EVs) and interacting with resident cells. MSC-derived EVs have emerged as promising therapeutic candidates for osteoarthritis (OA) because they carry bioactive molecules, are easily delivered, and exhibit low immunogenicity. In this study, we generated MSCs with altered cell fate by transferring the microenvironment of SW982 human synovial fibroblast-like cells through direct MSC-synovial fibroblast (SF) interaction and evaluated EVs derived from these cells (miSF-MSC-EVs) as a therapeutic strategy for OA. MSCs and SFs were stained with nuclear dyes, co-cultured for 48 h, and double-positive cells were isolated by fluorescence-activated cell sorting. Proteomic and next-generation sequencing analyses revealed enrichment of miRNAs associated with cell migration, adhesion, and transforming growth factor-β, Wnt, and PI3K signaling pathways in miSF-MSC-EVs. Compared with conventional MSC-EVs, miSF-MSC-EVs enhanced cell proliferation, improved regenerative responses, reduced inflammatory marker expression, and increased anti-inflammatory marker expression in vitro. Furthermore, miSF-MSC-EVs promoted cartilage repair in a mouse OA model, highlighting their potential as a regenerative therapeutic platform for OA treatment.
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Registered trials
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