Evidence map›Paper›PMID 38388473›Full record

ArticleArthritis research & therapy2024

Fibroblast-like synoviocytes-derived exosomal circFTO deteriorates rheumatoid arthritis by enhancing N6-methyladenosine modification of SOX9 in chondrocytes.

Guoqing Li, Yuxuan Fang, Nan Xu, Yimin Ding, Dan Liu

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Arthritis research & therapy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
4.7field-weighted citation impact, top 4% of its field
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

22 citing papers in PubMed, 20 citations in OpenAlex.

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  9. The significance of m6A-circFOXK2 in CD4Journal of translational autoimmunity · 2025
    Article
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  13. Crosstalk between N6-methyladenosine modification and ncRNAs in rheumatic diseases: therapeutic and diagnostic implications.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
    Review
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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

5 authors at 1 institution in 1 country.

Guoqing LiDepartment of Rheumatology and Immunology, Affiliated Hospital of Yangzhou University, Yangzhou University, Yangzhou, Jiangsu, 225000, China. guoqingyz@126.com.
Yuxuan FangDepartment of Rheumatology and Immunology, Affiliated Hospital of Yangzhou University, Yangzhou University, Yangzhou, Jiangsu, 225000, China.
Nan XuDepartment of Rheumatology and Immunology, Affiliated Hospital of Yangzhou University, Yangzhou University, Yangzhou, Jiangsu, 225000, China.
Yimin DingDepartment of Rheumatology and Immunology, Affiliated Hospital of Yangzhou University, Yangzhou University, Yangzhou, Jiangsu, 225000, China.
Dan LiuDepartment of Pathology, Affiliated Subei People's Hospital of Yangzhou University, Yangzhou, Jiangsu, 225000, China.
Yangzhou University · CN

Funding

Jiangsu Provincial Natural Science Foundation of China BK20201222National Natural Science Foundation of China 82071821The Fifth Phase of "333 Project" Scientific Research Project of Jiangsu Province in 2020 BRA2020175Yangzhou University "High-end Talent Plan" Top Talent Growth Plan (2019), and special fund for medical innovation and transformation of Yangzhou University AHYZUCXTD 202105
6 · The paper itself

Abstract

backgroundRheumatoid arthritis (RA) is a chronic inflammatory disease that causes disability worldwide. Exosomes released by fibroblast-like synoviocytes in RA (RA-FLSs-Exos) play a role in the development of RA, and circular RNAs (circRNAs) are important for RA progression. This study aimed to investigate the molecular mechanisms underlying the effects of RA-FLSs-Exos in RA and identify the potential pathway responsible for these effects.

methodsWe initially conducted microarray analysis to identify dysregulated circRNAs in exosomes associated with RA. We then co-cultured isolated RA-FLSs-Exos with chondrocytes to examine their role in RA. In vivo experiments were performed using collagen-induced arthritis mouse models, and circFTO knockdown was achieved through intra-articular injection of AAV5 vectors.

resultsOur findings revealed increased expression of circFTO in both RA-FLSs-Exos and synovial tissues from patients with RA. Exosomal circFTO hindered chondrocyte proliferation, migration, and anabolism while promoting apoptosis and catabolism. Mechanistically, we discovered that circFTO facilitates the formation of methyltransferases complex to suppress SRY-related high-mobility group box 9 (SOX9) expression with assistance from YTH domain family 2 (YTHDF2) through an m6A-dependent mechanism. Furthermore, inhibition of circFTO improved symptoms of RA in vivo.

conclusionTaken together, our study demonstrates that exosomal circFTO derived from FLSs contributes to the progression of RA by targeting SOX9. These findings highlight a promising target for treating RA.

Indexed as

Arthritis, RheumatoidSynoviocytesAnimalsCell ProliferationCells, CulturedChondrocytesFibroblastsHumansMiceRNA, CircularSOX9 Transcription FactorRNA, CircularSOX9 protein, humanSOX9 Transcription FactorcircRNAExosomeN6-methyladenosineRheumatoid arthritis

Identifiers

PMID38388473
PMCPMC10882813
OpenAlexW4392056142

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LicenceCC BY
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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.