Evidence map›Paper›PMID 41366047›Full record

ArticleScientific reports2025

Ubiquitin-specific protease 14 inhibition promotes mitophagy and attenuates neural apoptosis after spinal cord injury.

Dingwei Wu, Dehui Chen, Huina Chen, Zhengxi Yu, Hao Feng, Linquan Zhou, Zhi Chen, Tengbin Shi, Rongcan Wu, Yelei Zhang and 3 more

Abstract read
In one paragraph

Article in Scientific reports, 2025. 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

13 authors.

Dingwei Wu *Department of Orthopedics, Fujian Medical University Union Hospital, No.29, Xin Quan Road, Fuzhou, 350001, Fujian, China.
Dehui Chen *Department of Orthopedics, Fujian Medical University Union Hospital, No.29, Xin Quan Road, Fuzhou, 350001, Fujian, China.
Huina Chen *School of Health, Fujian Medical University, Fuzhou, 350108, Fujian, China.
Zhengxi YuDepartment of Orthopedics, Fujian Medical University Union Hospital, No.29, Xin Quan Road, Fuzhou, 350001, Fujian, China.
Hao FengDepartment of Orthopedics, Fujian Medical University Union Hospital, No.29, Xin Quan Road, Fuzhou, 350001, Fujian, China.
Linquan ZhouDepartment of Orthopedics, Fujian Medical University Union Hospital, No.29, Xin Quan Road, Fuzhou, 350001, Fujian, China.
Zhi ChenDepartment of Orthopedics, Fujian Medical University Union Hospital, No.29, Xin Quan Road, Fuzhou, 350001, Fujian, China.
Tengbin ShiDepartment of Orthopedics, Fujian Medical University Union Hospital, No.29, Xin Quan Road, Fuzhou, 350001, Fujian, China.
Rongcan WuDepartment of Orthopedics, Fujian Medical University Union Hospital, No.29, Xin Quan Road, Fuzhou, 350001, Fujian, China.
Yelei ZhangDepartment of Orthopedics, Fujian Medical University Union Hospital, No.29, Xin Quan Road, Fuzhou, 350001, Fujian, China.
Lei SunSchool of Health, Fujian Medical University, Fuzhou, 350108, Fujian, China.
Zhenyu WangDepartment of Orthopedics, Fujian Medical University Union Hospital, No.29, Xin Quan Road, Fuzhou, 350001, Fujian, China. zhenyu_wang@fjmu.edu.cn.ORCID 0009-0002-6679-9612
Wenge LiuDepartment of Orthopedics, Fujian Medical University Union Hospital, No.29, Xin Quan Road, Fuzhou, 350001, Fujian, China. wengeunion@fjmu.edu.cn.ORCID 0000-0002-3538-1646

Funding

Fujian Provincial Health Technology Project 2023CXA013Joint Funds for the innovation of Science and Technology,Fujian province 2021Y9041Natural Science Foundation of Fujian Province 2023J01758
6 · The paper itself

Abstract

Spinal cord injury (SCI) is a devastating condition characterized by severe neurological deficits and limited recovery, primarily due to the intricate cascade of secondary injury mechanisms. Post-SCI mitochondrial dysfunction can lead to increased oxidative stress and neuronal apoptosis. This study aimed to investigate whether inhibition of USP14 could enhance mitophagy, thereby counteracting apoptosis and providing effective neuroprotection both in vitro and in vivo after SCI. Pharmacological and genetic approaches were employed to inhibit USP14 in rat models of SCI and in HT-22 neuronal cells subjected to oxygen-glucose deprivation (OGD). The results revealed that USP14 inhibition significantly reduced neuronal apoptosis by modulating mitochondrial apoptotic pathways and preserving mitochondrial content, subsequently alleviating neurological deficits associated with SCI. Enhanced autophagic flux induced by USP14 inhibition facilitated selective clearance of damaged mitochondria, offering substantial protection to neurons and promoting functional motor recovery. Blocking mitophagy with 3-MA reversed these protective effects, underscoring the critical role of mitophagy in the neuroprotective outcomes mediated by USP14 inhibition. Collectively, our findings suggest that inhibiting USP14 enhances mitophagy, maintains mitochondrial function, and reduces neuronal apoptosis, thereby protecting neurons and improving motor function post-SCI. These results highlight USP14 as a promising therapeutic target for early intervention strategies in SCI through the modulation of mitochondrial function and enhancement of mitophagy.

Indexed as

ApoptosisMitophagyNeuronsSpinal Cord InjuriesUbiquitin ThiolesteraseAnimalsCell LineGlucoseMiceMitochondriaRatsRats, Sprague-DawleyGlucoseUbiquitin ThiolesteraseDUBsMitophagySpinal cord injuryUSP14USP14 inhibition

Identifiers

PMID41366047
PMCPMC12706073

What OpenQuestion holds

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LicenceCC BY-NC-ND
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Registered trials

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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.