Evidence map›Paper›PMID 38212777›Full record

ArticleEuropean journal of medical research2024

Identification of potential crucial genes and therapeutic targets for epilepsy.

Shitao Wang, Zhenrong Xie, Tian Jun, Xuelu Ma, Mengen Zhang, Feng Rao, Hui Xu, Jinghong Lu, Xiangqian Ding, Zongyou Li

Open access · goldAbstract read
In one paragraph

Article in European journal of medical research, 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, top 100% 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

1 citing paper in PubMed, 0 citations in OpenAlex.

  1. Deletion ofFrontiers in neurology
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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

10 authors at 3 institutions in 1 country.

Shitao WangDepartment of Neurology, Affiliated Fuyang People's Hospital of Anhui Medical University, Fuyang, 236000, Anhui, China. wangshitaomd@163.com.
Zhenrong XieThe Medical Biobank, First Affiliated Hospital of Kunming Medical University, Kunming, 650032, Yunnan, China.
Tian JunDepartment of Neurology, Affiliated Fuyang People's Hospital of Anhui Medical University, Fuyang, 236000, Anhui, China.
Xuelu MaDepartment of Neurology, Affiliated Fuyang People's Hospital of Anhui Medical University, Fuyang, 236000, Anhui, China.
Mengen ZhangDepartment of Neurology, Affiliated Fuyang People's Hospital of Anhui Medical University, Fuyang, 236000, Anhui, China.
Feng RaoDepartment of Neurology, Affiliated Fuyang People's Hospital of Anhui Medical University, Fuyang, 236000, Anhui, China.
Hui XuDepartment of Neurology, Affiliated Fuyang People's Hospital of Anhui Medical University, Fuyang, 236000, Anhui, China.
Jinghong LuDepartment of Neurology, Affiliated Fuyang People's Hospital of Anhui Medical University, Fuyang, 236000, Anhui, China.
Xiangqian DingDepartment of Neurosurgery, Qilu Hospital of Shandong University, Jinan, 250012, Shandong, China.
Zongyou LiDepartment of Neurology, Affiliated Fuyang People's Hospital of Anhui Medical University, Fuyang, 236000, Anhui, China.
Anhui Medical University · CNKunming Medical University · CNQilu Hospital of Shandong University · CN

Funding

Natural Science Foundation of Anhui Provincial Education Department 2022AH050756
6 · The paper itself

Abstract

backgroundEpilepsy, a central neurological disorder, has a complex genetic architecture. There is some evidence suggesting that genetic factors play a role in both the occurrence of epilepsy and its treatment. However, the genetic determinants of epilepsy are largely unknown. This study aimed to identify potential therapeutic targets for epilepsy.

methodsDifferentially expressed genes (DEGs) were extracted from the expression profiles of GSE44031 and GSE1834. Gene co-expression analysis was used to confirm the regulatory relationship between newly discovered epilepsy candidate genes and known epilepsy genes. Expression quantitative trait loci analysis was conducted to determine if epilepsy risk single-nucleotide polymorphisms regulate DEGs' expression in human brain tissue. Finally, protein-protein interaction analysis and drug-gene interaction analysis were performed to assess the role of DEGs in epilepsy treatment.

resultsThe study found that the protein tyrosine phosphatase receptor-type O gene (PTPRO) and the growth arrest and DNA damage inducible alpha gene (GADD45A) were significantly upregulated in epileptic rats compared to controls in both datasets. Gene co-expression analysis revealed that PTPRO was co-expressed with RBP4, NDN, PAK3, FOXG1, IDS, and IDS, and GADD45A was co-expressed with LRRK2 in human brain tissue. Expression quantitative trait loci analysis suggested that epilepsy risk single-nucleotide polymorphisms could be responsible for the altered PTPRO and GADD45A expression in human brain tissue. Moreover, the protein encoded by GADD45A had a direct interaction with approved antiepileptic drug targets, and GADD45A interacts with genistein and cisplatin.

conclusionsThe results of this study highlight PTPRO and GADD45A as potential genes for the diagnosis and treatment of epilepsy.

Indexed as

EpilepsyAnimalsGene Expression ProfilingHumansp21-Activated KinasesRatsRetinol-Binding Proteins, Plasmap21-Activated KinasesPAK3 protein, humanRBP4 protein, humanRetinol-Binding Proteins, PlasmaEpilepsyGADD45AGenePTPROTarget

Identifiers

PMID38212777
PMCPMC10782668
OpenAlexW4390742491

What OpenQuestion holds

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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.