Evidence map›Paper›PMID 40468839›Full record

ReviewExpert reviews in molecular medicine2025

Unveiling the Therapeutic Potential: Targeting Fibroblast-like Synoviocytes in Rheumatoid Arthritis.

Siran Yue, Junyu Fan, Duoli Xie, Chunhao Cao, Zhuqian Wang, Jie Huang, Fang Qiu, Xu Yang, Dongyi He, Aiping Lu and 1 more

Abstract readReview
In one paragraph

Review in Expert reviews in molecular medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
–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

24 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  4. [Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026
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  19. Frontier research on mechanisms of bone destruction in rheumatoid arthritis.Frontiers in cell and developmental biology · 2026
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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

11 authors.

Siran YueDepartment of Systems Biology, School of Life Sciences, Southern University of Science and Technology, Shenzhen, China.ORCID 0009-0001-7465-5486
Junyu FanDepartment of Systems Biology, School of Life Sciences, Southern University of Science and Technology, Shenzhen, China.
Duoli XieDepartment of Systems Biology, School of Life Sciences, Southern University of Science and Technology, Shenzhen, China.
Chunhao CaoDepartment of Systems Biology, School of Life Sciences, Southern University of Science and Technology, Shenzhen, China.
Zhuqian WangDepartment of Systems Biology, School of Life Sciences, Southern University of Science and Technology, Shenzhen, China.
Jie HuangDepartment of Systems Biology, School of Life Sciences, Southern University of Science and Technology, Shenzhen, China.
Fang QiuDepartment of Systems Biology, School of Life Sciences, Southern University of Science and Technology, Shenzhen, China.
Xu YangDepartment of Computational Biology, St. Jude Children's Research Hospital, Memphis, TN, USA.
Dongyi HeDepartment of Rheumatology, Guanghua Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Aiping LuInstitute of Integrated Bioinfomedicine and Translational Science (IBTS), School of Chinese Medicine, https://ror.org/0145fw131Hong Kong Baptist University, Hong Kong SAR, China.
Chao LiangDepartment of Systems Biology, School of Life Sciences, Southern University of Science and Technology, Shenzhen, China.ORCID 0000-0002-5617-3483

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Rheumatoid arthritis (RA) is a systemic autoimmune disease characterized by chronic inflammation of the synovial membrane, leading to cartilage destruction and bone erosion. Due to the complex pathogenesis of RA and the limitations of current therapies, increasing research attention has been directed towards novel strategies targeting fibroblast-like synoviocytes (FLS), which are key cellular components of the hyperplastic pannus. Recent studies have highlighted the pivotal role of FLS in the initiation and progression of RA, driven by their tumour-like transformation and the secretion of pro-inflammatory mediators, including cytokines, chemokines and matrix metalloproteinases. The aggressive phenotype of RA-FLS is marked by excessive proliferation, resistance to apoptosis, and enhanced migratory and invasive capacities. Consequently, FLS-targeted therapies represent a promising avenue for the development of next-generation RA treatments. The efficacy of such strategies - particularly those aimed at modulating FLS signalling pathways - has been demonstrated in both preclinical and clinical settings, underscoring their therapeutic potential. This review provides an updated overview of the pathogenic mechanisms and functional roles of FLS in RA, with a focus on critical signalling pathways under investigation, including Janus kinase/signal transducer and activator of transcription (JAK/STAT), mitogen-activated protein kinase (MAPK), nuclear factor kappa B (NF-κB), Notch and interleukin-1 receptor-associated kinase 4 (IRAK4). In addition, we discuss the emerging understanding of FLS-subset-specific contributions to immunometabolism and explore how computational biology is shaping novel targeted therapeutic strategies. A deeper understanding of the molecular and functional heterogeneity of FLS may pave the way for more effective and precise therapeutic interventions in RA.

Indexed as

Arthritis, RheumatoidFibroblastsSynoviocytesAnimalsHumansMolecular Targeted TherapySignal TransductionSynovial Membranefibroblast-like synoviocytespannusrheumatoid arthritissynoviumtargeted therapy

Identifiers

PMID40468839
PMCPMC12201960

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Registered trials

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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.