Evidence map›Paper›PMID 39430132›Full record

ReviewJournal of orthopaedic translation2024

Mitochondrial destabilization in tendinopathy and potential therapeutic strategies.

Linxiang Cheng, Qiangqiang Zheng, Kaijie Qiu, Dai Fei Elmer Ker, Xiao Chen, Zi Yin

Abstract readReview
In one paragraph

Review in Journal of orthopaedic translation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing 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

17 citing papers in PubMed.

  1. Article
  2. Article
  3. Engineered NestinJournal of extracellular vesicles · 2026
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Tendinopathy: The Interplay between Mechanical Stress, Inflammation, and Vascularity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Effect of High-Dose Vitamin C on Tendon Cell Degeneration-An In Vitro Study.International journal of molecular sciences · 2024
    Article
  17. 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

6 authors.

Linxiang ChengDepartment of Orthopedic Surgery of Sir Run Run Shaw Hospital, and Liangzhu Laboratory, Zhejiang University School of Medicine, Hangzhou, China.
Qiangqiang ZhengDepartment of Sports Medicine & Orthopedic Surgery, The Second Affiliated Hospital, And Liangzhu Laboratory, Zhejiang University School of Medicine, Hangzhou, China.
Kaijie QiuDepartment of Sports Medicine & Orthopedic Surgery, The Second Affiliated Hospital, And Liangzhu Laboratory, Zhejiang University School of Medicine, Hangzhou, China.
Dai Fei Elmer KerInstitute for Tissue Engineering and Regenerative Medicine, The Chinese University of Hong Kong, New Territories, Hong Kong.
Xiao ChenDepartment of Sports Medicine & Orthopedic Surgery, The Second Affiliated Hospital, And Liangzhu Laboratory, Zhejiang University School of Medicine, Hangzhou, China.
Zi YinDepartment of Orthopedic Surgery of Sir Run Run Shaw Hospital, and Liangzhu Laboratory, Zhejiang University School of Medicine, Hangzhou, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tendinopathy is a prevalent aging-related disorder characterized by pain, swelling, and impaired function, often resulting from micro-scarring and degeneration caused by overuse or trauma. Current interventions for tendinopathy have limited efficacy, highlighting the need for innovative therapies. Mitochondria play an underappreciated and yet crucial role in tenocytes function, including energy production, redox homeostasis, autophagy, and calcium regulation. Abnormalities in mitochondrial function may lead to cellular senescence. Within this context, this review provides an overview of the physiological functions of mitochondria in tendons and presents current insights into mitochondrial dysfunction in tendinopathy. It also proposes potential therapeutic strategies that focus on targeting mitochondrial health in tenocytes. These strategies include: (1) utilizing reactive oxygen species (ROS) scavengers to mitigate the detrimental effects of aberrant mitochondria, (2) employing mitochondria-protecting agents to reduce the production of dysfunctional mitochondria, and (3) supplementing with exogenous normal mitochondria. In conclusion, mitochondria-targeted therapies hold great promise for restoring mitochondrial function and improving outcomes in patients with tendinopathy.

Indexed as

AgingMitochondriaStem cellsTendinopathyTherapeutic strategies

Identifiers

PMID39430132
PMCPMC11488423

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.