Evidence map›Paper›PMID 40087281›Full record

ArticleBone research2025

SIRT3-PINK1-PKM2 axis prevents osteoarthritis via mitochondrial renewal and metabolic switch.

Yaoge Deng, Mingzhuang Hou, Yubin Wu, Yang Liu, Xiaowei Xia, Chenqi Yu, Jianfeng Yu, Huilin Yang, Yijian Zhang, Xuesong Zhu

Abstract read
In one paragraph

Article in Bone research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing 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

34 citing papers in PubMed.

  1. Review
  2. Article
  3. Persistent ZnAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  4. Review
  5. Microorganisms · 2026
    Article
  6. Review
  7. The ClockJournal of orthopaedic surgery and research · 2026
    Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. 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

10 authors.

Yaoge Deng *Department of Orthopaedics, The First Affiliated Hospital of Soochow University, Soochow University, Suzhou, 215006, China.
Mingzhuang Hou *Department of Orthopaedics, The First Affiliated Hospital of Soochow University, Soochow University, Suzhou, 215006, China.
Yubin Wu *Department of Orthopaedics, The First Affiliated Hospital of Soochow University, Soochow University, Suzhou, 215006, China.
Yang LiuDepartment of Orthopaedics, The First Affiliated Hospital of Soochow University, Soochow University, Suzhou, 215006, China.
Xiaowei XiaDepartment of Orthopaedics, The First Affiliated Hospital of Soochow University, Soochow University, Suzhou, 215006, China.
Chenqi YuDepartment of Orthopaedics, The First Affiliated Hospital of Soochow University, Soochow University, Suzhou, 215006, China.
Jianfeng YuDepartment of Orthopaedics, The First Affiliated Hospital of Soochow University, Soochow University, Suzhou, 215006, China.
Huilin YangDepartment of Orthopaedics, The First Affiliated Hospital of Soochow University, Soochow University, Suzhou, 215006, China. suzhouspine@163.com.
Yijian ZhangDepartment of Orthopaedics, The First Affiliated Hospital of Soochow University, Soochow University, Suzhou, 215006, China. zhangyijian@suda.edu.cn.
Xuesong ZhuDepartment of Orthopaedics, The First Affiliated Hospital of Soochow University, Soochow University, Suzhou, 215006, China. zhuxs@suda.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Maintaining mitochondrial homeostasis is critical for preserving chondrocyte physiological conditions and increasing resistance against osteoarthritis (OA). However, the underlying mechanisms governing mitochondrial self-renewal and energy production remain elusive. In this study, we demonstrated mitochondrial damage and aberrant mitophagy in OA chondrocytes. Genetically overexpressing PTEN-induced putative kinase 1 (PINK1) protects against cartilage degeneration by removing defective mitochondria. PINK1 knockout aggravated cartilage damage due to impaired mitophagy. SIRT3 directly deacetylated PINK1 to promote mitophagy and cartilage anabolism. Specifically, PINK1 phosphorylated PKM2 at the Ser127 site, preserving its active tetrameric form. This inhibited nuclear translocation and the interaction with β-catenin, resulting in a metabolic shift and increased energy production. Finally, a double-knockout mouse model demonstrated the role of the SIRT3-PINK1-PKM2 axis in safeguarding the structural integrity of articular joints and improving motor functions. Overall, this study provides a novel insight into the regulation of mitochondrial renewal and metabolic switches in OA.

Indexed as

Carrier ProteinsMembrane ProteinsMitochondriaOsteoarthritisProtein KinasesSirtuin 3Thyroid HormonesAnimalsChondrocytesHumansMaleMiceMice, Inbred C57BLMice, KnockoutMitophagyPTEN-Induced Putative KinaseCarrier ProteinsMembrane ProteinsPkm protein, mouseProtein KinasesPTEN-Induced Putative KinasePyruvate KinaseSirt3 protein, mouseSirtuin 3Thyroid Hormone-Binding ProteinsThyroid Hormones

Identifiers

PMID40087281
PMCPMC11909255

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.