Evidence map›Paper›PMID 38481810›Full record

ArticleInternational journal of biological sciences2024

The FTO-CMPK2 Pathway in Fibroblast-like Synoviocytes Modulates Rheumatoid Arthritis Synovial Inflammation and Cartilage Homeostasis via mtDNA Regulation.

Li Jin, Qiyue Chen, Ke Hu, Dandan Fan, Heping Zhang, Jiaxin Deng, Weizhong Qi, Qinghong Yu

Open access · goldAbstract read
In one paragraph

Article in International journal of biological sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
5.6field-weighted citation impact, top 3% 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

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

  1. Pooled it
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  4. mMolecular medicine reports · 2026
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  14. mFrontiers 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

8 authors at 1 institution in 1 country.

Li JinRheumatology and Clinical Imunology, ZhuJiang Hospital, Southern Medical University, 510280, Guangzhou, China.
Qiyue ChenTranslational Medicine Research Center, ZhuJiang Hospital, Southern Medical University, 510280, Guangzhou, China.
Ke HuRheumatology and Clinical Imunology, ZhuJiang Hospital, Southern Medical University, 510280, Guangzhou, China.
Dandan FanRheumatology and Clinical Imunology, ZhuJiang Hospital, Southern Medical University, 510280, Guangzhou, China.
Heping ZhangTranslational Medicine Research Center, ZhuJiang Hospital, Southern Medical University, 510280, Guangzhou, China.
Jiaxin DengRheumatology and Clinical Imunology, ZhuJiang Hospital, Southern Medical University, 510280, Guangzhou, China.
Weizhong QiTranslational Medicine Research Center, ZhuJiang Hospital, Southern Medical University, 510280, Guangzhou, China.
Qinghong YuRheumatology and Clinical Imunology, ZhuJiang Hospital, Southern Medical University, 510280, Guangzhou, China.
Zhujiang Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In rheumatoid arthritis (RA), a debilitating autoimmune disorder marked by chronic synovial inflammation and progressive cartilage degradation, fibroblast-like synoviocytes (FLS) are key pathogenic players. Current treatments targeting these cells are limited. Our study focused on the Fat Mass and Obesity-associated protein (FTO), known for its roles in cell proliferation and inflammatory response modulation, and its involvement in RA. We specifically examined the inflammatory regulatory roles of FTO and CMPK2, a mitochondrial DNA synthesis protein, in FLS. Utilizing a combination of in vitro and in vivo methods, including FTO inhibition and gene knockdown, we aimed to understand FTO's influence on RA progression and chondrocyte functionality. Our findings showed that increased FTO expression in RA synovial cells enhanced their proliferation and migration and decreased senescence and apoptosis. Inhibiting FTO significantly slowed the disease progression in our models. Our research also highlighted that the FTO-CMPK2 pathway plays a crucial role in regulating synovial inflammation through the mtDNA-mediated cGAS/STING pathway, affecting chondrocyte homeostasis. This study indicates that targeting the FTO-CMPK2 axis could be a promising new therapeutic strategy for managing RA.

Indexed as

Arthritis, RheumatoidSynoviocytesAlpha-Ketoglutarate-Dependent Dioxygenase FTOCartilageCell ProliferationCells, CulturedDNA, MitochondrialFibroblastsHomeostasisHumansInflammationSynovial MembraneAlpha-Ketoglutarate-Dependent Dioxygenase FTODNA, MitochondrialFTO protein, humanCMPK2FTOMitochondrial DNArheumatoid arthritissynovitis

Identifiers

PMID38481810
PMCPMC10929198
OpenAlexW4392011258

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.