Changes in the microglial phenotype drive neuroinflammation independent of systemic inflammation in the acute stage of heatstroke.
Overview
- Department of Tropical Medicine, Army Medical University, Chongqing, China
- Department of Neurology, Xinqiao Hospital, Army Medical University, Chongqing, China
Abstract
Heatstroke causes acute injury and damage across numerous organ systems, during this process, inflammation drives disease progression. In this study, we correlated temporal changes in inflammatory response with barrier breakdown within 24 h following heatstroke onset to explore whether inflammation in circulation can influence inflammation in brain. We found both pro-inflammatory cytokines expression and pathological lesions in tissue were elevated at 1 h and 6 h after heatstroke onset. However, by 24 h after heatstroke onset, while systemic inflammation was sustained at high levels, neuroinflammation and cerebral cortex damage had begun to reverse. The change in microglial phenotype from classic activation at 1 h to alternative activation at 24 h post heatstroke may explain the subsequent abatement of neuroinflammation. Taken together, our results may indicate microglial phenotype transformation drives neuroinflammation independent of systemic inflammation during the acute stage of heatstroke.
Reproduced under the paper's license (CC BY), from the paper cited above.
Code
The paper says that its authors' code is available on request: it was not published with the paper, so there is nothing to verify.
The paper's code and data availability statement is in the Data section.
Tracing map
A tracing map links a paper to the code its authors published: this paper has none (its code is available on request), so it has no map.
Data
No dataset and no data link were found in the paper.
Data and code availability
• All data reported in this paper will be shared by the lead contact upon request. • This paper does not report original code. • Any additional information required to reanalyze the reported in this paper is available from the lead contact upon request.
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 1, 30 September 2026: the first record
Recorded: type, language, journal, volume, issue, pages, dates, 9 authors, 1 keyword, 1 funder, 42 references, 11 RRIDs.
Cite
This paper
Li, P., Wang, Z., Liu, J., Wang, G., Luo, X., Luo, Z., Shen, T., He, G., & Yang, X. (2026). Changes in the microglial phenotype drive neuroinflammation independent of systemic inflammation in the acute stage of heatstroke. iScience, 29(4), 115254. https://
BibTeX
@article{li2026changes,
author = {Li, Ping and Wang, Zeze and Liu, Jun and Wang, Gong and Luo, Xue and Luo, Zhen and Shen, Tingting and He, Genlin and Yang, Xuesen},
title = {{Changes in the microglial phenotype drive neuroinflammation independent of systemic inflammation in the acute stage of heatstroke}},
journal = {iScience},
year = {2026},
month = mar,
volume = {29},
number = {4},
pages = {115254},
publisher = {Elsevier},
issn = {2589-0042},
doi = {10.1016/
url = {https://
pmid = {41959670},
pmcid = {PMC13058986}
}
RIS
TY - JOUR
AU - Li, Ping
AU - Wang, Zeze
AU - Liu, Jun
AU - Wang, Gong
AU - Luo, Xue
AU - Luo, Zhen
AU - Shen, Tingting
AU - He, Genlin
AU - Yang, Xuesen
TI - Changes in the microglial phenotype drive neuroinflammation independent of systemic inflammation in the acute stage of heatstroke
T2 - iScience
J2 - iScience
PY - 2026
DA - 2026/
VL - 29
IS - 4
SP - 115254
SN - 2589-0042
PB - Elsevier
DO - 10.1016/
UR - https://
LA - en
ER -
CSL-JSON
{
"id": "10.1016/
"type": "article-journal",
"title": "Changes in the microglial phenotype drive neuroinflammation independent of systemic inflammation in the acute stage of heatstroke",
"container-title": "iScience",
"author": [
{
"family": "Li",
"given": "Ping"
},
{
"family": "Wang",
"given": "Zeze"
},
{
"family": "Liu",
"given": "Jun"
},
{
"family": "Wang",
"given": "Gong"
},
{
"family": "Luo",
"given": "Xue"
},
{
"family": "Luo",
"given": "Zhen"
},
{
"family": "Shen",
"given": "Tingting"
},
{
"family": "He",
"given": "Genlin"
},
{
"family": "Yang",
"given": "Xuesen"
}
],
"container-title-short":
"volume": "29",
"issue": "4",
"page": "115254",
"DOI": "10.1016/
"PMID": "41959670",
"PMCID": "PMC13058986",
"ISSN": "2589-0042",
"publisher": "Elsevier",
"URL": "https://
"language": "en",
"issued": {
"date-parts": [
[
2026,
3,
6
]
]
}
}
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:
- Mesenchymal stem cell-derived extracellular vesicles ameliorate heat stroke-induced hippocampal injury and modulate VIM-AS1-associated miR-34a-5p/
Per2 signaling Journal: Frontiers in immunologyIn common: cellular / molecular, 4 references - [2] doi:10.3389/fphar.2026.1718110
- Protective role of miR-712-3p in heatstroke-induced brain injury: involvement of neuronal lysosomal function and association with astrocytic exosome-enriched preparations.Journal: Frontiers in pharmacologyIn common: cellular / molecular, 3 references
- [3] doi:10.1002/advs.202518421
- Modulation of miR-23b Wnt/
β-catenin Axis Strengthens Endothelial Barrier Properties. Journal: Advanced science (Weinheim, Baden-Wurttemberg, Germany)In common: cellular / molecular, 1 reference - [4] doi:10.1186/s40035-026-00565-1
- Plant-derived mitochondria mitigate aging-related neurodegeneration by reprogramming microglial mitochondrial energy metabolism.Journal: Translational neurodegenerationIn common: cellular / molecular, 1 reference
- [5] doi:10.1080/21505594.2026.2670939
- Integrated transcriptomic and proteomic analysis reveals inflammatory activation and blood-brain barrier disruption during meningitis-associated extraintestinal pathogenic &
lt;i& gt;Escherichia coli& lt;/ i& gt; infection. Journal: VirulenceIn common: cellular / molecular, 1 reference - [6] doi:10.1111/cbdd.70363
- Multi-Omics Integration Reveals That SN-011 Targets JUNB to Upregulate ADGRE5 and Restore Vascular Endothelial Cell Communication in Ischemic Stroke.Journal: Chemical biology & drug designIn common: cellular / molecular, 1 reference
- [7] doi:10.1371/journal.pone.0352334 [code]
- Dexamethasone restores blood-brain barrier integrity in an in vitro heatstroke model.Journal: PloS oneIn common: cellular / molecular, 1 reference
- [8] doi:10.1097/cm9.0000000000004019
- Transcranial photobiomodulation mitigates neuroinflammation by suppressing the activation of neurotoxic microglia through inhibition of the cGAS-STING pathway following intracerebral hemorrhage in mice.Journal: Chinese medical journalIn common: cellular / molecular, 1 reference
- [9] doi:10.3389/fnagi.2026.1787252
- Age-associated neuronal micronuclei formation and transfer to microglia.Journal: Frontiers in aging neuroscienceIn common: cellular / molecular, 1 reference
- [10] doi:10.1038/s41467-026-75522-7
- High ambient temperature activates a neural circuit for gut glucose uptake in male mice.Journal: Nature communicationsIn common: 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.
