Evidence map›Paper›PMID 41518574›Full record

ArticleScience China. Life sciences2026

TRIM21 contributes to senile osteoporosis by shifting the osteoadipogenic balance toward adipogenesis in BMSCs.

Changwei Li, Leilei Chang, Li Zhou, Zhou Dan, Minglong Qiu, Zhe Chen, Yong Chen, Guoqing Tang, Lianfu Deng

Abstract read
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In one paragraph

Article in Science China. Life sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Review
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

9 authors.

Changwei Li *Department of Orthopedics, Shanghai Key Laboratory for Prevention and Treatment of Bone and Joint Diseases, Shanghai Institute of Traumatology and Orthopedics, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China. lcw11876@rjh.com.cn.
Leilei Chang *Department of Orthopedics, Shanghai Key Laboratory for Prevention and Treatment of Bone and Joint Diseases, Shanghai Institute of Traumatology and Orthopedics, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China.
Li Zhou *Department of Orthopedics, Kunshan Hospital of Chinese Medicine, Affiliated Hospital of Yangzhou University, Suzhou, 215300, China.
Zhou DanDepartment of Orthopedics, Shanghai Key Laboratory for Prevention and Treatment of Bone and Joint Diseases, Shanghai Institute of Traumatology and Orthopedics, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China.
Minglong QiuDepartment of Orthopedics, Shanghai Key Laboratory for Prevention and Treatment of Bone and Joint Diseases, Shanghai Institute of Traumatology and Orthopedics, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China.
Zhe ChenDepartment of Orthopedics, Shanghai Key Laboratory for Prevention and Treatment of Bone and Joint Diseases, Shanghai Institute of Traumatology and Orthopedics, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China.
Yong ChenDepartment of Orthopedics, Kunshan Hospital of Chinese Medicine, Affiliated Hospital of Yangzhou University, Suzhou, 215300, China. doctorchen1976@163.com.
Guoqing TangDepartment of Orthopedics, Kunshan Hospital of Chinese Medicine, Affiliated Hospital of Yangzhou University, Suzhou, 215300, China. 17712485172@yzu.edu.cn.
Lianfu DengDepartment of Orthopedics, Shanghai Key Laboratory for Prevention and Treatment of Bone and Joint Diseases, Shanghai Institute of Traumatology and Orthopedics, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China. lfdeng@shsmu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

During aging, bone marrow stromal cells (BMSCs) tend to differentiate more into adipocytes than into osteoblasts, resulting in decreased bone formation and contributing to age-related osteoporosis and impaired bone regeneration. However, the molecular mechanisms underlying this process remain unclear. In this study, we observed an increase in the expression of TRIM21 in aged BMSCs, particularly those involved in adipogenesis. This increase in TRIM21 levels shifted the osteoadipogenic balance toward adipogenesis in BMSCs, resulting in reduced bone formation and ultimately leading to age-related osteoporosis and impaired bone regeneration. Mechanistically, activation of the IL-1β-JNK MAPK pathway triggered the expression of TRIM21 in aged BMSCs, which then shifted the osteoadipogenic balance toward adipogenesis by facilitating the degradation of β-catenin through K48 ubiquitination. Therefore, our findings suggest a potential intrinsic mechanism for age-related bone loss and suggest that targeting TRIM21 could be beneficial for treating age-related osteoporosis and impaired bone regeneration.

Indexed as

AdipogenesisMesenchymal Stem CellsOsteoporosisRibonucleoproteinsAdipocytesAgingAnimalsbeta CateninBone RegenerationCell DifferentiationCells, CulturedHumansInterleukin-1betaOsteogenesisSS-A AntigenTRIM21 Proteinbeta CateninInterleukin-1betaRibonucleoproteinsSS-A AntigenTRIM21 ProteinBMSCosteoadipogenic differentiationsenile bone regenerationsenile osteoporosisTRIM21

Identifiers

PMID41518574

What OpenQuestion holds

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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.