Evidence map›Paper›PMID 39846253›Full record

ArticleJCI insight2025

CD34hi subset of synovial fibroblasts contributes to fibrotic phenotype of human knee osteoarthritis.

Junya Miyahara, Yasunori Omata, Ryota Chijimatsu, Hiroyuki Okada, Hisatoshi Ishikura, Junya Higuchi, Naohiro Tachibana, Kosei Nagata, Shoichiro Tani, Kenichi Kono and 12 more

Abstract read
In one paragraph

Article in JCI insight, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

14 citing papers in PubMed.

  1. Article
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  6. European journal of nuclear medicine and molecular imaging · 2026
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  8. Review
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  11. Review
  12. Article
  13. Profiling synovial tissue reveals OA subgroups.Nature reviews. Rheumatology · 2025
    Article
  14. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

22 authors.

Junya MiyaharaSensory & Motor System Medicine.
Yasunori OmataSensory & Motor System Medicine.
Ryota ChijimatsuBone and Cartilage Regenerative Medicine.
Hiroyuki OkadaSensory & Motor System Medicine.
Hisatoshi IshikuraSensory & Motor System Medicine.
Junya HiguchiSensory & Motor System Medicine.
Naohiro TachibanaSensory & Motor System Medicine.
Kosei NagataSensory & Motor System Medicine.
Shoichiro TaniSensory & Motor System Medicine.
Kenichi KonoSensory & Motor System Medicine.
Kohei KawaguchiSensory & Motor System Medicine.
Ryota YamagamiSensory & Motor System Medicine.
Hiroshi InuiSensory & Motor System Medicine.
Shuji TaketomiSensory & Motor System Medicine.
Yasuhide IwanagaSensory & Motor System Medicine.
Asuka TerashimaBone and Cartilage Regenerative Medicine.
Fumiko YanoBone and Cartilage Regenerative Medicine.
Masahide SekiLaboratory of Systems Genomics, Department of Computational Biology and Medical Sciences, The University of Tokyo, Kashiwa, Japan.
Yutaka SuzukiLaboratory of Systems Genomics, Department of Computational Biology and Medical Sciences, The University of Tokyo, Kashiwa, Japan.
Roland BaronDepartment of Medicine, Harvard Medical School and Endocrine Unit, MGH, Boston, Massachusetts, USA.
Sakae TanakaSensory & Motor System Medicine.
Taku SaitoSensory & Motor System Medicine.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Osteoarthritis (OA) shows various clinical manifestations depending on the status of its joint components. We aimed to identify the synovial cell subsets responsible for OA pathophysiology by comprehensive analyses of human synovium samples in single-cell resolution. Two distinct OA synovial tissue groups were classified by gene expression profiles in RNA-Seq: inflammatory and fibrotic. The inflammatory group exhibited high expression of inflammatory cytokines, histologically inflammatory infiltrate, and a more severe pain score. The fibrotic group showed higher expression of fibroblast growth factor (FGFs) and bone morphogenetic proteins (BMPs), showed histologically perivascular fibrosis, and showed a lower pain score. In single-cell RNA-Seq (scRNA-Seq) of synovial cells, MERTKloCD206lo macrophages and CD34hi fibroblasts were associated with the inflammatory and fibrotic groups, respectively. Among the 3 fibroblast subsets, CD34loTHY1lo and CD34loTHY1hi fibroblasts were influenced by synovial immune cells, whereas CD34hi fibroblasts were influenced by mural and endothelial cells. Particularly, in CD34hi fibroblast subsets, CD34hiCD70hi fibroblasts promoted proliferation of Tregs, potentially suppressing synovitis and protecting articular cartilage. Elucidation of the mechanisms underlying the regulation of these synovial cell subsets may lead to novel strategies for OA therapeutics.

Indexed as

Antigens, CD34FibroblastsOsteoarthritis, KneeSynovial MembraneAgedFemaleFibrosisHumansMacrophagesMaleMiddle AgedPhenotypeAntigens, CD34Bone biologyInflammationOsteoarthritis

Identifiers

PMID39846253
PMCPMC11790023

What OpenQuestion holds

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Registered trials

None linked

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.