Evidence map›Paper›PMID 40374649›Full record

ArticleNature communications2025

Regulating obesity-induced osteoarthritis by targeting p53-FOXO3, osteoclast ferroptosis, and mesenchymal stem cell adipogenesis.

Chen Zhao, Keyu Kong, Pengcheng Liu, Xuzhuo Chen, Kewei Rong, Pu Zhang, Lei Wang, Xiaoqing Wang

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing 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

27 citing papers in PubMed.

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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.

Chen Zhao *Department of Orthopedics, Shanghai Key Laboratory of Orthopedics Implant, the Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.ORCID http://orcid.org/0000-0001-7323-8237
Keyu Kong *Department of Orthopedics, Shanghai Key Laboratory of Orthopedics Implant, the Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Pengcheng LiuDepartment of Orthopedics, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Xuzhuo ChenDepartment of Oral Surgery, Shanghai Key Laboratory of Stomatology & Shanghai Research Institute of Stomatology, National Clinical Research Center for Oral Diseases, Shanghai Ninth People's Hospital, College of Stomatology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Kewei RongDepartment of Orthopedics, Shanghai Key Laboratory of Orthopedics Implant, the Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Pu ZhangDepartment of Orthopedics, Shanghai Key Laboratory of Orthopedics Implant, the Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Lei WangDepartment of Orthopedics, Shanghai Key Laboratory of Orthopedics Implant, the Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. wanglei12041986@163.com.ORCID http://orcid.org/0000-0001-5232-1541
Xiaoqing WangDepartment of Orthopedics, Shanghai Key Laboratory of Orthopedics Implant, the Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. osteoclast2006@163.com.ORCID http://orcid.org/0000-0003-0051-1241

Funding

National Natural Science Foundation of China (National Science Foundation of China) 81871791National Natural Science Foundation of China (National Science Foundation of China) 81902194
6 · The paper itself

Abstract

Obesity-related osteoarthritis (OA) and the molecular mechanisms governing multiple joint structural changes that occur with obesity are not well understood. This study investigated the progression of obesity in mice and validated the results using human joint samples post-arthroplasty. The results show that obesity is associated with the degeneration of the cartilage layer and abnormal remodeling of the subchondral bone layer, and this occurs alongside aging and DNA damage in chondrocytes, osteoclasts, and stem cells. Regulation of p53-FOXO3 gene loop expression in response to DNA damage effectively inhibits chondrocyte apoptosis, catabolism, and excessive osteoclast differentiation, while the intra-articular delivery of a lentivirus expressing FOXO3 to mouse joints alleviates the progression of OA. The excessive differentiation of subchondral bone marrow osteoclasts is ferroptosis-dependent and driven by the senescence-associated secretory phenotype. The results have identified multiple potential targets for future research into the progression of obesity-related OA.

Indexed as

AdipogenesisFerroptosisForkhead Box Protein O3Mesenchymal Stem CellsObesityOsteoarthritisOsteoclastsTumor Suppressor Protein p53AnimalsCell DifferentiationChondrocytesDNA DamageHumansMaleMiceMice, Inbred C57BLForkhead Box Protein O3FOXO3 protein, humanFoxO3 protein, mouseTrp53 protein, mouseTumor Suppressor Protein p53

Identifiers

PMID40374649
PMCPMC12081733

What OpenQuestion holds

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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 OpenQuestion graph.