Evidence map›Paper›PMID 39363112›Full record

ArticleExperimental & molecular medicine2024

FTO-mediated SMAD2 m6A modification protects cartilage against Osteoarthritis.

Hongyi Zhou, Ziang Xie, Yu Qian, Weiyu Ni, Lei Cui, Xiangqian Fang, Shuanglin Wan, Xiangde Zhao, An Qin, Shunwu Fan and 1 more

Abstract read
In one paragraph

Article in Experimental & molecular medicine, 2024. 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. Review
  2. Article
  3. mMolecular medicine reports · 2026
    Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. The Role ofBiomolecules · 2025
    Review
  11. Article
  12. Review
  13. Review
  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

11 authors.

Hongyi Zhou *Department of Orthopaedic Surgery, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Ziang Xie *Department of Orthopaedic Surgery, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Yu Qian *Department of Orthopaedics and Traumatology, The First Affiliated Hospital of Zhejiang Chinese Medical University (Zhejiang Provincial Hospital of Chinese Medicine), Hangzhou, China.
Weiyu NiDepartment of Orthopaedic Surgery, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Lei CuiCollaborative Innovation Centre of Regenerative Medicine and Medical BioResource Development and Application Co-constructed by the Province and Ministry, Guangxi Medical University, Nanning, China.
Xiangqian FangDepartment of Orthopaedic Surgery, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Shuanglin WanDepartment of Orthopaedic Surgery, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Xiangde ZhaoDepartment of Orthopaedic Surgery, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, China.
An QinDepartment of Orthopaedics, Shanghai Key Laboratory of Orthopaedic Implants, Shanghai Ninth People's Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China. dr_qinan@163.com.ORCID 0000-0002-8785-8848
Shunwu FanDepartment of Orthopaedic Surgery, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, China. shunwu_fan@zju.edu.cn.ORCID 0000-0003-3443-4395
Yizheng WuDepartment of Orthopaedic Surgery, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, China. yizheng_wu@zju.edu.cn.

Funding

China Postdoctoral Science Foundation 2022M720125National Natural Science Foundation of China (National Science Foundation of China) 81972089National Natural Science Foundation of China (National Science Foundation of China) 82000837National Natural Science Foundation of China (National Science Foundation of China) 82102591National Natural Science Foundation of China (National Science Foundation of China) 82302730National Natural Science Foundation of China (National Science Foundation of China) 82372440
6 · The paper itself

Abstract

N6-methyladenosine (m6A) modification is one of the most prevalent forms of epigenetic modification and plays an important role in the development of degenerative diseases such as osteoarthritis (OA). However, the evidence concerning the role of m6A modification in OA is insufficient. Here, m6A modification was increased in human OA cartilage and degenerated chondrocytes. Among all of the m6A enzymes, the expression of the demethylase fat mass and obesity-associated protein (FTO) decreased dramatically. Conditional knockout of FTO in chondrocytes accelerates OA progression. FTO transcription is regulated by runt-related transcription factor-1 (RUNX1). Reduced FTO elevates m6A modification at the adenosine N6 position in SMAD family member 2 (SMAD2) mRNA, whose stability is subsequently modulated by the recruited m6A reader protein YTH N6-methyladenosine RNA binding protein F2 (YTHDF2). Collectively, these findings reveal the function and mechanism of the m6A family member FTO in OA progression. Therefore, reducing m6A modification to increase SMAD2 stability by activating FTO might be a potential therapeutic strategy for OA treatment.

Indexed as

AdenosineAlpha-Ketoglutarate-Dependent Dioxygenase FTOChondrocytesOsteoarthritisSmad2 ProteinAnimalsCartilageGene Expression RegulationHumansMaleMiceRNA-Binding ProteinsAdenosineAlpha-Ketoglutarate-Dependent Dioxygenase FTOFTO protein, humanN-methyladenosineRNA-Binding ProteinsSmad2 ProteinSMAD2 protein, human

Identifiers

PMID39363112
PMCPMC11542000

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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.