Evidence map›Paper›PMID 41193790›Full record

ArticleMolecular neurobiology2025

Beyond Impaired GABAergic Signaling: Inflammation and Metabolic Dysfunction in Genetic Epilepsy Induced by GABRG2 Mutation.

Dingding Shen, Wenwen Wu, Jing Zhou, Xin Zhang, Longwu Zhan, Peipei Qian, Jingjing Qian, Aisong Guo, Aihong Li, Qi Zhang

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular neurobiology, 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. 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

10 authors.

Dingding Shen *Department of Neurology in Affiliated Hospital of Nantong University, Jiangsu Key Laboratory of Tissue Engineering and Neuroregeneration, Key Laboratory of Neuroregeneration of Ministry of Education, Medical school, Co-innovation Center of Neuroregeneration, Nantong University, Nantong, China.
Wenwen Wu *Jiangsu Key Laboratory of Tissue Engineering and Neuroregeneration, Key Laboratory of Neuroregeneration of Ministry of Education, Co-innovation Center of Neuroregeneration, Nantong University, Nantong, China.
Jing Zhou *Jiangsu Key Laboratory of Tissue Engineering and Neuroregeneration, Key Laboratory of Neuroregeneration of Ministry of Education, Co-innovation Center of Neuroregeneration, Nantong University, Nantong, China.
Xin ZhangJiangsu Key Laboratory of Tissue Engineering and Neuroregeneration, Key Laboratory of Neuroregeneration of Ministry of Education, Co-innovation Center of Neuroregeneration, Nantong University, Nantong, China.
Longwu ZhanJiangsu Key Laboratory of Tissue Engineering and Neuroregeneration, Key Laboratory of Neuroregeneration of Ministry of Education, Co-innovation Center of Neuroregeneration, Nantong University, Nantong, China.
Peipei QianClinical Medical Research Center, The Third Affiliated Hospital of Soochow University, Changzhou, China, Changzhou, China.
Jingjing QianDepartment of Ophthalmology, Affiliated Hospital of Nantong University, Nantong, China.
Aisong GuoDepartment of Traditional Chinese Medicine, Affiliated Hospital of Nantong University, Nantong, China.
Aihong LiDepartment of Neurology in Affiliated Hospital of Nantong University, Jiangsu Key Laboratory of Tissue Engineering and Neuroregeneration, Key Laboratory of Neuroregeneration of Ministry of Education, Medical school, Co-innovation Center of Neuroregeneration, Nantong University, Nantong, China. 15851205508@163.com.
Qi ZhangDepartment of Neurology in Affiliated Hospital of Nantong University, Jiangsu Key Laboratory of Tissue Engineering and Neuroregeneration, Key Laboratory of Neuroregeneration of Ministry of Education, Medical school, Co-innovation Center of Neuroregeneration, Nantong University, Nantong, China. zhangqi@ntu.edu.cn.

Funding

National Natural Science Foundation of China 82271487National Natural Science Foundation of China 82371460Postgraduate Research & Practice Innovation Program of Jiangsu Province KYCX23_3385Scientific Research Project of The Health Commission of Jiangsu Province ZDB2020003Scientific Research Projects of Nantong City MS2022035Scientific Research Projects of Nantong City MS2023081Scientific Research Projects of Nantong City MSZ19054
6 · The paper itself

Abstract

Although the mechanisms underlying genetic epilepsies associated with mutations in the γ-aminobutyric acid type A receptor γ2 subunit gene (GABRG2) have been extensively investigated, prior studies primarily focused on the functional alterations of mutant ion channels. Emerging evidence has indicated that neuroinflammation and metabolic disturbances are involved in acquired epilepsies. To further investigate the potential involvement of these mechanisms in genetic epilepsies, we generated a transgenic zebrafish line, Tg(hGABRG2

Indexed as

Epilepsygamma-Aminobutyric AcidInflammationMutationReceptors, GABA-ASignal TransductionAnimalsAnimals, Genetically ModifiedBrainHEK293 CellsHumansZebrafishgamma-Aminobutyric AcidReceptors, GABA-AC–C chemokine receptor type 2 (CCR2) antagonistGenetic epilepsyInflammatoryMetabolic dysfunctionγ-aminobutyric acid (GABAA) receptor γ2 subunit gene (GABRG2)

Identifiers

PMID41193790

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.