Evidence map›Paper›PMID 42246142›Full record

ArticleInternational journal of rheumatic diseases2026

Reciprocal Regulation of GLI1 and GLI3 Fine Tunes the Pathogenic Behavior of Synovial Fibroblasts in Rheumatoid Arthritis.

Motohiko Sato, Tetsuya Saito, Yoji Komiya, Seiji Noda, Yasuhiro Tagawa, Akio Yamamoto, Hideyuki Iwai, Kentaro Endo, Hideyuki Koga, Yasuhiro Takahara and 5 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of rheumatic diseases, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

15 authors.

Motohiko SatoDepartment of Rheumatology, Graduate School of Medical and Dental Sciences, Institute of Science Tokyo (IST), Tokyo, Japan.ORCID https://orcid.org/0009-0000-2475-0437
Tetsuya SaitoDepartment of Rheumatology, Graduate School of Medical and Dental Sciences, Institute of Science Tokyo (IST), Tokyo, Japan.ORCID https://orcid.org/0009-0003-7241-6662
Yoji KomiyaDepartment of Rheumatology, Graduate School of Medical and Dental Sciences, Institute of Science Tokyo (IST), Tokyo, Japan.
Seiji NodaDepartment of Rheumatology, Graduate School of Medical and Dental Sciences, Institute of Science Tokyo (IST), Tokyo, Japan.ORCID https://orcid.org/0000-0003-0268-8446
Yasuhiro TagawaDepartment of Rheumatology, Graduate School of Medical and Dental Sciences, Institute of Science Tokyo (IST), Tokyo, Japan.
Akio YamamotoDepartment of Rheumatology, Graduate School of Medical and Dental Sciences, Institute of Science Tokyo (IST), Tokyo, Japan.ORCID https://orcid.org/0000-0002-2866-6571
Hideyuki IwaiDepartment of Rheumatology, Graduate School of Medical and Dental Sciences, Institute of Science Tokyo (IST), Tokyo, Japan.
Kentaro EndoCenter for Stem Cell and Regenerative Medicine, Institute of Science Tokyo (IST), Tokyo, Japan.ORCID https://orcid.org/0000-0003-4790-4632
Hideyuki KogaDepartment of Joint Surgery and Sports Medicine, Graduate School of Medical and Dental Sciences, Institute of Science Tokyo (IST), Tokyo, Japan.
Yasuhiro TakaharaDepartment of Orthopedic Surgery, Nippon Kokan Fukuyama Hospital, Hiroshima, Japan.
Kazutaka SugimotoDepartment of Orthopedics, Sonodakai Joint Replacement Center Hospital, Tokyo, Japan.
Ichiro SekiyaCenter for Stem Cell and Regenerative Medicine, Institute of Science Tokyo (IST), Tokyo, Japan.ORCID https://orcid.org/0000-0002-6331-722X
Eiryo KawakamiDepartment of Artificial Intelligence Medicine, Graduate School of Medicine, Chiba University, Chiba, Japan.
Tadashi HosoyaDepartment of Rheumatology, Graduate School of Medical and Dental Sciences, Institute of Science Tokyo (IST), Tokyo, Japan.
Shinsuke YasudaDepartment of Rheumatology, Graduate School of Medical and Dental Sciences, Institute of Science Tokyo (IST), Tokyo, Japan.

Funding

Japan Agency for Medical Research and Development 21ek0410061h0003Japan Society for the Promotion of Science London 21K20755Japan Society for the Promotion of Science London 22K08519
6 · The paper itself

Abstract

objectiveWe investigated the role of GLI3, a transcription factor highly expressed in the pathogenic THY1

methodsGLI3 protein levels were quantified in freshly isolated RASF subsets by Western blotting. Bulk RASFs were subjected to siRNA-mediated knockdown (KD) of GLI3 or GLI1, followed by RNA sequencing. The effects of GANT61 on RASF proliferation, cell-cycle progression, migration, viability, and apoptosis were assessed using EdU/PI analysis, scratch assays, CCK-8 assays, and Annexin V/PI flow cytometry.

resultsGLI3 expression was enriched in THY1

conclusionGLI3 functions as a negative regulator of GLI1 and its downstream targets that drive the pathogenic behavior of RASFs. Targeting the GLI1-GLI3 axis may represent a promising therapeutic strategy to modulate fibroblast-driven inflammation and joint destruction in RA.

Indexed as

Arthritis, RheumatoidFibroblastsNerve Tissue ProteinsSynovial MembraneZinc Finger Protein GLI1Zinc Finger Protein Gli3ApoptosisCell MovementCell ProliferationCells, CulturedGene Expression RegulationHumansPyridinesPyrimidinesSignal TransductionGANT 61GLI1 protein, humanGLI3 protein, humanNerve Tissue ProteinsPyridinesPyrimidinesZinc Finger Protein GLI1Zinc Finger Protein Gli3fibroblastGLI1GLI3hedgehog signaling pathwayrheumatoid arthritis

Identifiers

PMID42246142
PMCPMC13238299

What Socratic holds

Textmetadata
LicenceCC BY
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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 Socratic graph.