Pantothenic Acid Protects Neurons After Ischemic Stroke by Targeting ID3 to Restore Action Potential Amplitude.
Overview
- Department of Neurology, The First Affiliated Hospital of Guangxi University of Science and Technology, Liuzhou City, Guangxi Zhuang Autonomous Region, China
- Department of Neurology, The First Affiliated Hospital of Guangxi Medical University, Nanning City, Guangxi Zhuang Autonomous Region, China
Abstract
Ischemic stroke (IS) remains a devastating condition with limited neuroprotective options. This study investigated the role of the transcription factor inhibitor of DNA binding 3 (ID3) in acute IS through an integrated approach. Combining bioinformatic analysis of Gene Expression Omnibus (GEO) datasets with machine learning (ML) algorithms, we identified ID3 as a consistently downregulated key gene, and its expression level correlated with neurological severity. Functional analysis suggested ID3 modulates neuroinflammation. Furthermore, ID3 and C‐type lectin domain family 4 member E (CLEC4E) showed potential as diagnostic biomarkers. Using network pharmacology, pantothenic acid (PA) was predicted as a potential ID3‐targeting drug. This was preliminarily tested in an oxygen–glucose deprivation/
Reproduced under the paper's license (CC BY), from the paper cited above.
Code
The paper links to its data, not to its authors' code: see the Data section.
Tracing map
A tracing map links a paper to the code its authors published: this paper has none, so it has no map.
Data
Datasets cited
- geo:GSE16561, at NCBI GEO; found in “Data Availability Statement”
Data Availability Statement
The publicly available datasets (GSE16561 (https://
Reproduced under the paper's license (CC BY), from the paper cited above.
Versions
The history of this record: each version stored by the harvester or made by a correction of its authors or of the maintainers of its code, and what changed in its facts. The texts of the paper (its abstract, its availability statements) are not part of it; versions that changed only those are not listed.
Version 2, 28 September 2026
- Publisher: n/a → Wiley
Version 1, 27 September 2026: the first record
Recorded: type, language, journal, volume, issue, pages, dates, 6 authors, 5 keywords, 8 MeSH terms, 1 funder, 40 references.
Cite
This paper
Chen, H., Chen, M., Meng, L., Wei, X., Qin, Y., & Bi, Z. (2026). Pantothenic Acid Protects Neurons After Ischemic Stroke by Targeting ID3 to Restore Action Potential Amplitude. Journal of neuroscience research, 104(5), e70130. https://
BibTeX
@article{chen2026pantoth
author = {Chen, Hongqiao and Chen, Mingli and Meng, Lian and Wei, Xing and Qin, Yan and Bi, Zhumei},
title = {{Pantothenic Acid Protects Neurons After Ischemic Stroke by Targeting ID3 to Restore Action Potential Amplitude}},
journal = {Journal of neuroscience research},
year = {2026},
month = may,
volume = {104},
number = {5},
pages = {e70130},
publisher = {Wiley},
issn = {0360-4012},
doi = {10.1002/
url = {https://
pmid = {42130286},
pmcid = {PMC13172942}
}
RIS
TY - JOUR
AU - Chen, Hongqiao
AU - Chen, Mingli
AU - Meng, Lian
AU - Wei, Xing
AU - Qin, Yan
AU - Bi, Zhumei
TI - Pantothenic Acid Protects Neurons After Ischemic Stroke by Targeting ID3 to Restore Action Potential Amplitude
T2 - Journal of neuroscience research
J2 - J Neurosci Res
PY - 2026
DA - 2026/
VL - 104
IS - 5
SP - e70130
SN - 0360-4012
PB - Wiley
DO - 10.1002/
UR - https://
LA - en
ER -
CSL-JSON
{
"id": "10.1002/
"type": "article-journal",
"title": "Pantothenic Acid Protects Neurons After Ischemic Stroke by Targeting ID3 to Restore Action Potential Amplitude",
"container-title": "Journal of neuroscience research",
"author": [
{
"family": "Chen",
"given": "Hongqiao"
},
{
"family": "Chen",
"given": "Mingli"
},
{
"family": "Meng",
"given": "Lian"
},
{
"family": "Wei",
"given": "Xing"
},
{
"family": "Qin",
"given": "Yan"
},
{
"family": "Bi",
"given": "Zhumei"
}
],
"container-title-short":
"volume": "104",
"issue": "5",
"page": "e70130",
"DOI": "10.1002/
"PMID": "42130286",
"PMCID": "PMC13172942",
"ISSN": "0360-4012",
"publisher": "Wiley",
"URL": "https://
"language": "en",
"issued": {
"date-parts": [
[
2026,
5,
1
]
]
}
}
Similar papers
The papers with a page that share the most with this one: the tools found in their code, their categories, datasets, cited references and authors, the rarest counting most.
- [1] doi:10.1038/s44321-026-00473-x
- OTUB1 non-canonically inhibits TAB2 ubiquitination to govern microglia-mediated neuroinflammation.Journal: EMBO molecular medicineIn common: NCBI GEO GSE16561, mouse, cellular / molecular, 1 reference
- [2] doi:10.3389/fmolb.2026.1844734
- Discovery and validation of programmed cell death-associated key biomarker genes in ischemic stroke via ssGSEA/
WGCNA and LASSO-SVM-RFE. Journal: Frontiers in molecular biosciencesIn common: NCBI GEO GSE16561, stroke - [3] doi:10.1007/s10571-026-01710-0
- The Role and Diagnostic Efficacy of the METTL14/
GADD45B m& lt;sup& gt;6& lt;/ sup& gt;A Methylation/ BDNF Regulatory Axis in Acute Ischemic Stroke. Journal: Cellular and molecular neurobiologyIn common: NCBI GEO GSE16561, stroke - [4] doi:10.1186/s12951-026-04551-7
- The role of AI-assisted drug repurposing in neurological disorders: a systematic review of validation strategies, challenges and opportunities.Journal: Journal of nanobiotechnologyIn common: NCBI GEO GSE16561
- [5] doi:10.3389/fphar.2026.1870571
- Tissue-autonomous pharmacological direction: how target expression landscapes convert balanced compounds into tissue-selective agents.Journal: Frontiers in pharmacologyIn common: NCBI GEO GSE16561
- [6] doi:10.1038/s41419-026-09021-4
- ACLY alleviates cerebral ischemia/
reperfusion injury by reducing oxidative stress and enhancing mitochondrial function via histone acetylation. Journal: Cell death & diseaseIn common: stroke, mouse, cellular / molecular, 1 reference - [7] doi:10.1002/jev2.70295
- RVG-Modified BMSCs-Derived Small Extracellular Vesicles Loaded With miR-21 Alleviate Neuronal Injury Resulted From Excessive Autophagy via Targeting PTEN/
Akt/ mTOR Pathway After Cerebral Ischaemia. Journal: Journal of extracellular vesiclesIn common: stroke, mouse, cellular / molecular, 1 reference - [8] doi:10.1016/j.isci.2026.115779
- Propranolol alleviates cerebral infarction through the β2-AR-mediated ERK/
NLRP3 pathway. Journal: iScienceIn common: stroke, mouse, cellular / molecular, 1 reference - [9] doi:10.1097/md.0000000000048634
- Identifying therapeutic target genes for stroke through systematic druggable Mendelian randomization analysis.Journal: MedicineIn common: stroke, cellular / molecular, 1 reference
- [10] doi:10.3389/fimmu.2026.1790415 [code]
- Machine learning-based identification of concomitant stroke and prognostic analysis in patients with Guillain-Barré syndrome: a retrospective study.Journal: Frontiers in immunologyIn common: stroke, 1 reference
Contribute
The authors of this paper can claim it, correct its record and validate its tracing map, and the maintainers of its code (its owner, or a public member of its organization) correct what it says of their repository; anyone signed in can ask for its removal. Every request goes to OSCR's own machine, which answers it; your account page follows them.
Sign in with ORCID to claim this paper as one of its authors, correct its record or validate its tracing map: when the paper's metadata lists your ORCID iD, you are recognized at once. Maintainers of its code: sign in with GitHub, then claim the repository on your account page.
Claim this paper
Correct its record
Say what each link of this record is, remove the ones that are not the paper's, add the ones that are missing. The correction becomes a new version of the record, in its Versions section.
Request its removal
To ask OSCR to remove this record, the copies of its authors' scripts or its tracing map, use the removal request page: signed in, you say who you are, what to remove and why, then review and confirm the request. Published rules decide every request (how).
Discussion, reproductions, activity
Discussion: questions and error reports about this paper and its code, from signed-in readers and its authors. It opens with sign-in.
Reproductions: reports from readers who ran the authors' code: what they reproduced, with which environment, commit and data. It opens with sign-in.
Activity: what happens around this paper: new versions of its record, its map's validation, discussions and reproductions. It opens with sign-in.
