Evidence map›Paper›PMID 36453412›Full record

ArticleNeural regeneration research2023

Neuronal nitric oxide synthase/reactive oxygen species pathway is involved in apoptosis and pyroptosis in epilepsy.

Xiao-Xue Xu, Rui-Xue Shi, Yu Fu, Jia-Lu Wang, Xin Tong, Shi-Qi Zhang, Na Wang, Mei-Xuan Li, Yu Tong, Wei Wang and 4 more

Open access · goldAbstract read
In one paragraph

Article in Neural regeneration research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.1field-weighted citation impact, top 7% 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

19 citing papers in PubMed, 37 citations in OpenAlex.

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  16. The lactate metabolism and protein lactylation in epilepsy.Frontiers in cellular neuroscience · 2024
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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

14 authors at 5 institutions in 1 country.

Xiao-Xue XuDepartment of Pharmaceutical Toxicology, School of Pharmaceutical Science, China Medical University; Department of Neurology, The First Affiliated Hospital of China Medical University, Shenyang, Liaoning Province, China.
Rui-Xue ShiDepartment of Pharmaceutical Toxicology, School of Pharmaceutical Science, China Medical University, Shenyang, Liaoning Province, China.
Yu FuDepartment of Pharmaceutical Toxicology, School of Pharmaceutical Science, China Medical University, Shenyang, Liaoning Province, China.
Jia-Lu WangDepartment of Neurology, The First Affiliated Hospital of China Medical University, Shenyang, Liaoning Province, China.
Xin TongDepartment of Pharmaceutical Toxicology, School of Pharmaceutical Science, China Medical University, Shenyang, Liaoning Province, China.
Shi-Qi ZhangDepartment of Pharmaceutical Toxicology, School of Pharmaceutical Science, China Medical University, Shenyang, Liaoning Province, China.
Na WangKey Laboratory of Medical Electrophysiology, Ministry of Education & Medical Electrophysiological Key Laboratory of Sichuan Province, Institute of Cardiovascular Research, Southwest Medical University, Luzhou, Sichuan Province, China.
Mei-Xuan LiDepartment of Pharmaceutical Toxicology, School of Pharmaceutical Science, China Medical University, Shenyang, Liaoning Province, China.
Yu TongDepartment of Pharmaceutical Toxicology, School of Pharmaceutical Science, China Medical University, Shenyang, Liaoning Province, China.
Wei WangDepartment of Endocrinology and Metabolism, The Fourth Affiliated Hospital of China Medical University, Shenyang, Liaoning Province, China.
Miao HeDepartment of Pharmaceutical Toxicology, School of Pharmaceutical Science, China Medical University, Shenyang, Liaoning Province, China.
Bing-Yang LiuDepartment of Endocrinology, Shengjing Hospital of China Medical University, Shenyang, Liaoning Province, China.
Gui-Lan ChenKey Laboratory of Medical Electrophysiology, Ministry of Education & Medical Electrophysiological Key Laboratory of Sichuan Province, Institute of Cardiovascular Research, Southwest Medical University, Luzhou, Sichuan Province, China.
Feng GuoDepartment of Pharmaceutical Toxicology, School of Pharmaceutical Science, China Medical University, Shenyang, Liaoning Province, China.
China Medical University · CNShenyang Pharmaceutical University · CNSouthwest Medical University · CNFirst Hospital of China Medical University · CNFourth Affiliated Hospital of China Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dysfunction of neuronal nitric oxide synthase contributes to neurotoxicity, which triggers cell death in various neuropathological diseases, including epilepsy. Studies have shown that inhibition of neuronal nitric oxide synthase activity increases the epilepsy threshold, that is, has an anticonvulsant effect. However, the exact role and potential mechanism of neuronal nitric oxide synthase in seizures are still unclear. In this study, we performed RNA sequencing, functional enrichment analysis, and weighted gene coexpression network analysis of the hippocampus of tremor rats, a rat model of genetic epilepsy. We found damaged hippocampal mitochondria and abnormal succinate dehydrogenase level and Na

Indexed as

apoptosisbioinformatics analysiscell deathepilepsynitric oxide synthaseoxidative stresspyroptosisRNA sequencingTremor ratweighted gene co-expression network analysis

Identifiers

PMID36453412
PMCPMC9838157
OpenAlexW4310023551

What Socratic holds

Textmetadata
LicenceCC BY-NC-SA
Read underepoch 390

Registered trials

None linked

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 Socratic graph.