Evidence map›Paper›PMID 38865079›Full record

ArticleMolecular neurobiology2025

20-Deoxyingenol Activates Mitophagy Through TFEB and Promotes Functional Recovery After Spinal Cord Injury.

Chenyu Wu, Yu Chen, Ximiao Chen, Yekai Zhang, Xiaoying Zhao, Yuxin Deng, Chenchao Li, Di Zhang, Xiaolei Zhang, Sheng Wang

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. 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.

Chenyu Wu *Department of Orthopaedics, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Zhejiang Province, Wenzhou, China.
Yu Chen *Department of Orthopaedics, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Zhejiang Province, Wenzhou, China.
Ximiao Chen *Department of Orthopaedics, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Zhejiang Province, Wenzhou, China.
Yekai ZhangDepartment of Orthopaedics, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Zhejiang Province, Wenzhou, China.
Xiaoying ZhaoDepartment of Orthopaedics, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Zhejiang Province, Wenzhou, China.
Yuxin DengDepartment of Orthopaedics, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Zhejiang Province, Wenzhou, China.
Chenchao LiDepartment of Orthopaedics, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Zhejiang Province, Wenzhou, China.
Di ZhangDepartment of Orthopaedics, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Zhejiang Province, Wenzhou, China. zhangdi@wmu.edu.cn.
Xiaolei ZhangDepartment of Orthopaedics, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Zhejiang Province, Wenzhou, China. zhangxiaolei@wmu.edu.cn.
Sheng WangDepartment of Orthopaedics, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Zhejiang Province, Wenzhou, China. wangthomas2002@163.com.

Funding

Wenzhou Science and Technology Bureau Foundation Y2020056Zhejiang Provincial Natural Science Foundation of China LQ23H060002
6 · The paper itself

Abstract

Spinal cord injury (SCI) can lead to permanent paralysis and various motor, sensory and autonomic nervous system dysfunction. The complex pathophysiological processes limit the effectiveness of many clinical treatments. Mitochondria has been reported to play a key role in the pathogenesis of SCI; while mitophagy is a protective mechanism against mitochondrial dysfunction. However, there is recently little drugs that may targeted activate mitophagy to treat SCI. In this study, we evaluated the role of 20-Deoxyingenol (20-DOI) in SCI and explored its potential mechanisms. We used a SCI rat model and evaluated the functional outcomes after the injury. Western blotting and immunofluorescence techniques were used to analyze the levels of mitophagy, apoptosis, and TFEB-related signaling pathways. Our research results show that 20-DOI significantly improves the apoptosis of neural cells after TBHP stimulation and functional recovery after spinal cord injury. In addition, mitophagy, TFEB levels, and apoptosis are related to the mechanism of 20-DOI treatment for spinal cord injury. Specifically, our research results indicate that 20-DOI restored the autophagic flux after injury, thereby inducing mitophagy, eliminating the accumulation of Cyto C, and inhibiting apoptosis. Further mechanism research suggests that 20-DOI may regulate mitophagy by promoting TFEB nuclear translocation. These results indicate that 20-DOI can significantly promote recovery after spinal cord injury, which may be a promising treatment method for spinal cord injury.

Indexed as

ApoptosisBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsMitophagyRats, Sprague-DawleyRecovery of FunctionSpinal Cord InjuriesAnimalsMaleMitochondriaNeuronsRatsSignal TransductionBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsTFEB protein, rat20-DeoxyingenolApoptosisAutophagyMitophagySpinal cord injuryTFEB

Identifiers

PMID38865079

What Socratic holds

Textmetadata
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 Socratic graph.