Evidence map›Paper›PMID 39671271›Full record

ArticleJournal of cellular and molecular medicine2024

TLR3 Knockdown Attenuates Pressure-Induced Neuronal Damage In Vitro.

Li Lin, Zhongzhong Lv, Chao Zhou, Taiyang Zhu, Yuting Hu, Xiaoyu Sun, Hui Zhou, Miao Wang, Yongtao Lin, Guoqing Gu and 5 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of cellular and molecular medicine, 2024. 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. 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

15 authors.

Li LinDepartment of Neurology, Xuzhou Medical University, Xuzhou, China.ORCID 0009-0006-0234-3404
Zhongzhong LvDepartment of Neurosurgery, Benq Hospital Affiliated to Nanjing Medical University, Nanjing, China.
Chao ZhouDepartment of Neurology, Xuzhou Medical University, Xuzhou, China.
Taiyang ZhuDepartment of Neurology, Xuzhou Medical University, Xuzhou, China.
Yuting HuDepartment of Neurology, Xuzhou Medical University, Xuzhou, China.
Xiaoyu SunDepartment of Neurology, Xuzhou Medical University, Xuzhou, China.
Hui ZhouDepartment of Neurology, Xuzhou Medical University, Xuzhou, China.
Miao WangDepartment of Neurology, Xuzhou Medical University, Xuzhou, China.
Yongtao LinXuzhou Medical University, Xuzhou, China.
Guoqing GuXuzhou Medical University, Xuzhou, China.
Shang WangDepartment of Neurology, Xuzhou Medical University, Xuzhou, China.
Yan ZhouDepartment of Neurology, Xuzhou Medical University, Xuzhou, China.
Jingjing HanDepartment of Neurology, Xuzhou Medical University, Xuzhou, China.
Guoliang JinDepartment of Neurology, Xuzhou Medical University, Xuzhou, China.
Fang HuaDepartment of Neurology, Xuzhou Medical University, Xuzhou, China.

Funding

Jiangsu Education Committee, China Since 2012
6 · The paper itself

Abstract

The disruption of nerve parenchyma and axonal networks triggered by spinal cord injury (SCI) can initiate a cascade of events associated with secondary injury. Toll-like receptors play a critical role in initiating and regulating immune-inflammatory responses following SCI; however, the precise involvement of Toll-like receptor-3 (TLR3) in secondary neuronal injury remains incompletely understood. To investigate the potential contribution of TLR3 in mediating neuronal pressure-induced damage, we established a stress-induced neuronal damage model using rat anterior horn motor neuron line (VSC4.1), which was subjected to varying levels and durations of sustained pressure. Our findings suggest that pressure induces neuronal damage and apoptosis, and reduced proliferation rates in VSC4.1 cells. Furthermore, this pressure-induced neuronal injury is accompanied by upregulation of TLR3 expression and activation of downstream TLR3 signalling molecules. Knockdown experiments targeting TLR3 significantly alleviate pressure-induced motor neuron injury and apoptosis within the anterior horn region while promoting mitochondria-related autophagy and reducing mitochondrial dysfunction via the TLR3/IRF3 and TLR3/NF-κB pathways.

Indexed as

ApoptosisAutophagyGene Knockdown TechniquesPressureToll-Like Receptor 3AnimalsCell LineCell ProliferationMitochondriaMotor NeuronsNeuronsNF-kappa BRatsSignal TransductionSpinal Cord InjuriesNF-kappa BTLR3 protein, ratToll-Like Receptor 3apoptosisautophagymicrotubule‐associated protein‐2mitochondriapressure‐injuredspinal cord injuryTLR3

Identifiers

PMID39671271
PMCPMC11640903

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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.