Evidence map›Paper›PMID 39838674›Full record

ArticleCurrent gene therapy2025

Plasmalogens Activate AKT/mTOR Signaling to Attenuate Reactive Oxygen Species Production in Spinal Cord Injury.

Mengdan Cheng, Yan Gao, Yiqing Wu, Liangliang Zhang, Bai Xu, Xiaojie Lu

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Article in Current gene therapy, 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

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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. Article
4 · The record

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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.

Mengdan ChengNeuroscience Center, Wuxi School of Medicine, Jiangnan University, Wuxi, Jiangsu Province, 214122, PR China.ORCID 0009-0004-7230-3737
Yan GaoNeuroscience Center, Wuxi School of Medicine, Jiangnan University, Wuxi, Jiangsu Province, 214122, PR China.
Yiqing WuNeuroscience Center, Wuxi School of Medicine, Jiangnan University, Wuxi, Jiangsu Province, 214122, PR China.
Liangliang ZhangThoracic Surgery Department, Handan Central Hospital, Handan, Hebei Province, 050011, PR China.
Bai XuNeuroscience Center, Wuxi School of Medicine, Jiangnan University, Wuxi, Jiangsu Province, 214122, PR China.
Xiaojie LuNeuroscience Center, Wuxi School of Medicine, Jiangnan University, Wuxi, Jiangsu Province, 214122, PR China.

Funding

National Natural Science Foundation of China 82072791
6 · The paper itself

Abstract

backgroundPlasmalogens, the primary phospholipids in the brain, possess intrinsic antioxidant properties and are crucial components of the myelin sheath surrounding neuronal axons. While their neuroprotective effects have been demonstrated in Alzheimer's disease, their potential benefits in spinal cord injury remain unexplored. This study investigates the reparative effects of plasmalogens on spinal cord injury and the underlying mechanisms.

methodsIn vitro, we developed dorsal root ganglion (DRG) and RAW 264.7 cell models under high-reactive oxygen species (ROS) conditions to assess ROS levels, neuronal damage, and inflammatory microenvironment changes before and after plasmalogen application. In vivo, we used a complete mouse spinal cord transection model to evaluate changes in ROS levels, neuronal demyelination, and apoptosis following plasmalogen treatment. Additionally, we assessed sensory and motor function recovery and investigated the regulatory effects of plasmalogens on the AKT/mTOR signaling pathway.

resultsIn high-ROS cell models, plasmalogens protected DRG neurons (TUJ-1) from axonal damage and modulated the proinflammatory/anti-inflammatory balance in RAW 264.7 cells. In vivo, plasmalogens significantly reduced ROS levels, improved the immune microenvironment, decreased the proinflammatory (iNOS)/anti-inflammatory (ARG-1) ratio, lowered neuronal (TUJ-1) apoptosis (Caspase-3, BAX), and reduced axonal degeneration while promoting myelin (MBP) regeneration, indicating a neuroprotective effect. These findings are linked to the activation of the AKT/mTOR signaling pathway.

conclusionPlasmalogens reduce ROS levels and regulate inflammation-induced damage, contributing to neuroprotection. This study reveals that plasmalogens promote remyelination, reduce axonal degeneration and neuronal apoptosis, and-used here for the first time in spinal cord injury repair- may protect neurons by reducing ROS levels and activating the AKT/mTOR signaling pathway.

Indexed as

PlasmalogensProto-Oncogene Proteins c-aktReactive Oxygen SpeciesSpinal Cord InjuriesTOR Serine-Threonine KinasesAnimalsApoptosisDisease Models, AnimalGanglia, SpinalMiceNeuronsNeuroprotective AgentsRAW 264.7 CellsSignal TransductionmTOR protein, mouseNeuroprotective AgentsPlasmalogensProto-Oncogene Proteins c-aktReactive Oxygen SpeciesTOR Serine-Threonine KinasesAKT/mTORneuronal apoptosisPlasmalogensROSspinal cord injurytrauma.

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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.