Evidence map›Paper›PMID 38281257›Full record

ArticleMolecular biology reports2024

The CSF1-CSF1R pathway in the trigeminal ganglion mediates trigeminal neuralgia via inflammatory responses in mice.

Zile He, Chao Xu, Jiaqi Guo, Tianyu Liu, Yunpeng Zhang, Yi Feng

Abstract read
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In one paragraph

Article in Molecular biology reports, 2024. 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
0.3field-weighted citation impact, top 45% of its field
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 citations in OpenAlex.

  1. Review
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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

6 authors at 3 institutions in 2 countries.

Zile He *Department of Anesthesiology, Peking University People's Hospital, Xizhimen South Street 11, Beijing, 100044, China.ORCID http://orcid.org/0000-0002-3499-9022
Chao Xu *Department of Anesthesiology, Zhongshan Hospital, Fudan University, Shanghai, China.ORCID http://orcid.org/0000-0001-8000-106X
Jiaqi Guo *Shanghai Minhang Center for Disease Control and Prevention, Shanghai, China.ORCID http://orcid.org/0009-0009-9968-7714
Tianyu LiuDepartment of Anesthesiology, Peking University People's Hospital, Xizhimen South Street 11, Beijing, 100044, China.ORCID http://orcid.org/0000-0002-6769-5690
Yunpeng ZhangDepartment of Anesthesiology, Peking University People's Hospital, Xizhimen South Street 11, Beijing, 100044, China.ORCID http://orcid.org/0000-0003-1552-2250
Yi FengDepartment of Anesthesiology, Peking University People's Hospital, Xizhimen South Street 11, Beijing, 100044, China. doctor_yifeng@sina.com.ORCID http://orcid.org/0000-0002-3952-1351
Peking University · CNShanghai Municipal Center For Disease Control Prevention · CNSun Yat-sen University · CN

Funding

National Key Research and Development Program of China No.2018YFC2001905
6 · The paper itself

Abstract

backgroundTrigeminal neuralgia (TN) is the most severe type of neuropathic pain. The trigeminal ganglion (TG) is a crucial target for the pathogenesis and treatment of TN. The colony-stimulating factor 1 (CSF1) - colony-stimulating factor 1 receptor (CSF1R) pathway regulates lower limb pain development. However, the effect and mechanism of the CSF1-CSF1R pathway in TG on TN are unclear.

methodsPartial transection of the infraorbital nerve (pT-ION) model was used to generate a mouse TN model. Mechanical and cold allodynia were used to measure pain behaviors. Pro-inflammatory factors (IL-6, TNF-a) were used to measure inflammatory responses in TG. PLX3397, an inhibitor of CSF1R, was applied to inhibit the CSF1-CSF1R pathway in TG. This pathway was activated in naïve mice by stereotactic injection of CSF1 into the TG.

resultsThe TN model activated the CSF1-CSF1R pathway in the TG, leading to exacerbated mechanical and cold allodynia. TN activated inflammatory responses in the TG manifested as a significant increase in IL-6 and TNF-a levels. After using PLX3397 to inhibit CSF1R, CSF1R expression in the TG declined significantly. Inhibiting the CSF1-CSF1R pathway in the TG downregulated the expression of IL-6 and TNF-α to reduce allodynia-related behaviors. Finally, mechanical allodynia behaviors were exacerbated in naïve mice after activating the CSF1-CSF1R pathway in the TG.

conclusionsThe CSF1-CSF1R pathway in the TG modulates TN by regulating neuroimmune responses. Our findings provide a theoretical basis for the development of treatments for TN in the TG.

Indexed as

Macrophage Colony-Stimulating FactorNeuralgiaReceptors, Granulocyte-Macrophage Colony-Stimulating FactorTrigeminal NeuralgiaAminopyridinesAnimalsHyperalgesiaInterleukin-6MicePyrrolesReceptor Protein-Tyrosine KinasesTrigeminal GanglionAminopyridinesCSF1 protein, mouseCsf1r protein, mouseInterleukin-6Macrophage Colony-Stimulating FactorpexidartinibPyrrolesReceptor Protein-Tyrosine KinasesReceptors, Granulocyte-Macrophage Colony-Stimulating FactorColony-stimulating factorInflammationTrigeminal ganglionTrigeminal neuralgia

Identifiers

PMID38281257
OpenAlexW4391289666

What OpenQuestion holds

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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.