ArticleOsteoarthritis and cartilage2026
Inhibition of fibroblast activation protein partially restores the homeostatic phenotype of mechanoactivated synoviocytes.
Article in Osteoarthritis and cartilage, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
Abstract
objectiveSynovial fibrosis, characterized by mechanoactivation of fibroblast-like synoviocytes (FLS), is thought to be a driver of osteoarthritis (OA). Fibroblast activation protein (FAP) is expressed by activated FLS and contributes to OA progression, but the mechanisms by which it does so are undefined. The objective of this study was to evaluate FAP expression in OA across species, assess FAP regulation in FLS, and determine how FAP inhibition alters the phenotype of mechanoactivated FLS.
methodsSynovium from human patients (n = 9) and animal models of OA (murine n = 5; porcine n = 8) was evaluated for FAP expression via immunofluorescence. An in vitro model of FLS mechanoactivation was established by plating FLS on polyacrylamide gels or glass +/-TGFβ (n = 5/group). Activated FLS were treated with a FAP inhibitor (FAPi) and phenotype was evaluated via immunofluorescence, RT-qPCR, collagen gel contraction, and FUNCAT (n = 5-7/group).
resultsFAP was increased in mouse (MD: 10.3, 95% CI: [3.0, 17.6]), pig (8.7 [4.6, 12.8]), and human (24.5 [11.8, 37.3]) OA synovium and correlated with histological markers of synovial pathology. In vitro culture on stiff substrates activated FLS, and treatment with TGFβ induced FAP expression (1.8 [0.3, 3.4]). FAP inhibition partially rescued the morphological, transcriptional, and functional profile of activated FLS (e.g., reduced stress fiber formation (-0.2 [-0.35, -0.05]), αSMA expression (-2.9 [-4.9, -0.84], and contractility (-0.16 [-0.33, -0.0]).
conclusionsThe upregulation of FAP in OA synovium is conserved across species. FAP is a TGFβ-responsive driver of FLS mechanoactivation, and its inhibition partially restores the homeostatic function of FLS. Targeting FAP may represent a novel strategy to improve synovial health and mitigate joint degeneration in OA.
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.