ArticleArthritis research & therapy2026
Mesenchymal stem cell exosomes alleviate osteoarthritis by inhibiting complement activation via a CD59-dependent pathway.
Article in Arthritis research & therapy, 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
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
- Plasma Proteomics Reveals Persistent and Surgery-Responsive Molecular Signatures in Osteoarthritis Patients.International journal of molecular sciences · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMesenchymal stromal/stem cell (MSC) exosomes were previously shown to be effective in alleviating joint pain and degeneration in a rat model of temporomandibular joint osteoarthritis (TMJ-OA). However, the role of MSC exosomes in regulating complement activity implicated in OA inflammation remains to be elucidated. Here, we investigate the effects of MSC exosomes on the assembly of terminal complement complex, C5b-9, and its associated inflammation and matrix degradation in TMJ-OA.
methodsFollowing TMJ-OA induction, the rats received 3 weekly intra-articular injections of MSC exosomes or phosphate-buffered saline (PBS). The sham animals were given needle pricks. At 4-weeks post-treatment, tissue samples were harvested for transcriptomic profiling, micro-computed tomography (micro-CT), histology, immunohistochemistry, histomorphometry, C5b-9 enzyme-linked immunosorbent assay (ELISA), and multiplex cytokine analyses. Chondrocyte cultures were used to assess the effects of MSC exosomes on complement serum-induced chondrocyte inflammation and matrix degradation. The role of exosomal CD59 on complement assembly was also evaluated through neutralization with an anti-CD59 antibody.
resultsWe observed that MSC exosomes mediated joint repair by suppressing pain and inflammation, reducing fibrosis and matrix degradation, and restoring the condylar cartilage and subchondral bone. Concurrently, there was suppressed complement activity with exosome treatment, as evidenced by the reduced levels of C5b-9 in the condylar cartilage and overlying synovium, and preferential synovial mRNA expression of complement inhibitors over effectors. These were accompanied by the decreased levels of pro-inflammatory cytokines such as IL-12 (p70), IL-17 A, IFN-γ, IL-18, and MIP-3α, and increased levels of anti-inflammatory cytokines including IL-2, IL-4, and IL-10 in the synovium with exosome treatment. Using chondrocyte cultures, we attributed the suppression of OA inflammation and matrix degradation to exosomal CD59, which inhibits complement activation. Specifically, MSC exosomes reduced C5b-9 formation and complement-induced inflammatory gene expression and MMP13 secretion in chondrocytes, and these effects were abrogated upon neutralization with an anti-CD59 antibody.
conclusionsThese findings demonstrated that MSC exosomes alleviate OA inflammation and matrix degradation by inhibiting complement activity via a CD59-dependent pathway.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.