Evidence map›Paper›PMID 39004783›Full record

ArticleCNS neuroscience & therapeutics2024

Therapeutic effects of exendin-4 on spinal cord injury via restoring autophagy function and decreasing necroptosis in neuron.

Xiao Gao, Qu-Peng Li, Jing-Ru Hao, Kai Sun, Hu Feng, Kai-Jin Guo, Can Gao

Abstract read
In one paragraph

Article in CNS neuroscience & therapeutics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. MicroRNA-582-5p modulation of UBR5 affects inflammatory response and motor recovery after spinal cord injury.European spine journal : official publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society · 2026
    Article
  2. Review
  3. Review
  4. 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

7 authors.

Xiao GaoNanjing Medical University, Nanjing, China.ORCID 0009-0004-0511-6923
Qu-Peng LiDepartment of Orthopedics, The Affiliated Hospital of Xuzhou Medical University, Xuzhou Medical University, Xuzhou, China.
Jing-Ru HaoNMPA Key Laboratory for Research and Evaluation of Narcotic and Psychotropic Drugs, Jiangsu Province Key Laboratory of Anesthesiology, Jiangsu Province Key Laboratory of Anesthesia and Analgesia Application, Xuzhou Medical University, Xuzhou, China.
Kai SunNanjing Medical University, Nanjing, China.
Hu FengDepartment of Orthopedics, The Affiliated Hospital of Xuzhou Medical University, Xuzhou Medical University, Xuzhou, China.
Kai-Jin GuoNanjing Medical University, Nanjing, China.
Can GaoNanjing Medical University, Nanjing, China.ORCID 0000-0001-5552-9639

Funding

General program of Xuzhou Science and Technology Bureau KC23268Key laboratory open project of Xuzhou Medical University XZSYSKF2023004National Natural Science Foundation of China 82171199National Natural Science Foundation of China 82371215
6 · The paper itself

Abstract

aimsNecroptosis is one of programmed death that may aggravate spinal cord injury (SCI). We aimed to investigate the effect and mechanism of exendin-4 (EX-4) on the recovery of motor function and necroptosis after SCI.

methodsThe SD rats with left hemisection in the T10 spinal cord as SCI model were used. The behavior tests were measured within 4 weeks. The effects of EX-4 on necroptosis-associated proteins and autophagy flux were explored. In addition, the SHSY5Y cell model was introduced to explore the direct effect of EX-4 on neurons. The effect of lysosome was explored using mTOR activator and AO staining.

resultsEX-4 could improve motor function and limb strength, promote the recovery of autophagy flux, and accelerate the degradation of necroptosis-related protein at 3 d after injury in rats. EX-4 reduced lysosome membrane permeability, promoted the recovery of lysosome function and autophagy flux, and accelerated the degradation of necroptosis-related proteins by inhibiting the phosphorylation level of mTOR in the SHSY5Y cell model.

conclusionOur results demonstrated that EX-4 may improve motor function after SCI via inhibiting mTOR phosphorylation level and accelerating the degradation of necroptosis-related proteins in neurons. Our findings may provide new therapeutic targets for clinical treatment after SCI.

Indexed as

AutophagyExenatideNecroptosisNeuronsRats, Sprague-DawleySpinal Cord InjuriesAnimalsCell Line, TumorHumansMaleNeuroprotective AgentsRatsRecovery of FunctionTOR Serine-Threonine KinasesExenatideNeuroprotective AgentsTOR Serine-Threonine Kinasesautophagy fluxexendin‐4hemisectionnecroptosisSHSY5Y cellspinal cord injury

Identifiers

PMID39004783
PMCPMC11246977

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.