ArticleCell reports. Medicine2025
Mesothelin as a biomarker and potential therapeutic target in rheumatoid arthritis bone destruction.
Article in Cell reports. Medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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
2 citing papers in PubMed.
- Precision medicine in rheumatoid arthritis: advances and clinical applications of multi-omics biomarkers.Frontiers in immunology · 2026Review
- M1 macrophage-targeted engineered ginseng stems and leaves-derived extracellular vesicles delivery system for alleviating rheumatoid arthritis.Regenerative biomaterials · 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
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mesothelin (MSLN) is implicated in multiple biological processes, notably in modulating immune responses. However, the role of MSLN in osteoclastogenesis remains underexplored. Here we reveal that the level of MSLN was significantly elevated in rheumatoid arthritis (RA) patients, as well as in collagen-induced arthritis (CIA) animals. Pharmacological and genetic inhibition of MSLN significantly impair osteoclast differentiation and bone resorption. In the animal model, down-regulation of MSLN effectively alleviates bone destruction. Further investigation unravels that MSLN directly interacts with phosphatidylinositol 3-kinase (PI3K), resulting in the activation of the PI3K/protein kinase B (AKT) signaling pathway, which subsequently induces the expression and translocation of nuclear factor of activated T cells 1 (NFATc1), thereby promoting osteoclast differentiation. Overall, our findings indicate that MSLN could serve as a valuable prognostic marker for bone destruction in RA, and targeting MSLN may offer a therapeutic strategy for RA-related bone destruction.
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.