OSCR

SLC22A3 deficiency leads to cognitive impairment through the cardio-neuroinflammatory axis mediated HA/H1R/NLRP3 pathway in heart failure mice.

Overview

Authors: Zhitian Wang1, Lv Zhou1, Na Zhao1, Tianxiao Li1, Fan Geng1, Jingting Kong1, Yahao Zhang2, Zhijun Zhang1, Qing-Guo Ren1
  1. Department of Neurology, Zhongda Hospital, School of Medicine, Jiangsu Provincial Key Laboratory of Brain Science and Medicine, Southeast University, Nanjing, 210009, China
  2. Department of Cardiology, National Key Clinical Specialty, Zhongda Hospital, Southeast University, Nanjing, 210009, China
Journal: Redox biology, volume 92, article 104127
Dates: received 13 February 2026; accepted 12 March 2026; published online 12 March 2026; in print May 2026
Type: Research article · Language: English
License: CC BY-NC-ND
Identifiers: DOI 10.1016/j.redox.2026.104127 · PMID 41833108 · PMCID PMC12999320 · OpenAlex W7135097099
Open access: gold, a free copy (OpenAlex)
Status: data only
Categories: human (organism), mouse (organism), Alzheimer's / dementia (population), cellular / molecular (subfield)
Methods: Statistics, Evoked potentials
Keywords: Heart failure, Cognitive impairment, Cardio-neuroinflammatory axis, SLC22A3, Histamine, NLRP3 inflammasome
MeSH: Cognitive Dysfunction*, Heart Failure*, Histamine*, Neuroinflammatory Diseases*, NLR Family, Pyrin Domain-Containing 3 Protein*, Animals, Blood-Brain Barrier, Disease Models, Animal, Humans, Male, Mice, Mice, Knockout, Organic Cation Transporter 3, Signal Transduction (* major topic)
Topic: Inflammasome and immune disorders (Molecular Biology, Biochemistry, Genetics and Molecular Biology), according to OpenAlex
Funding: Research Personnel Cultivation Programme of Zhongda Hospital; Southeast University (CZXM-GSP-RC121); Jiangsu Province High-Level Hospital Construction Funds (GSP-LCYJFH07)
Citations: not cited yet (Europe PMC); 70 references in the paper

Abstract

The abstract is not reproduced here: the paper's license (CC BY-NC-ND) does not allow it. Read it in the paper, at the publisher or on Europe PMC.

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

Data links

Data availability statement

The paper has a data availability statement. Its license (CC BY-NC-ND) does not allow reproducing it here; in short, from what the harvester recognized in it:

  • no repository, dataset or request procedure was recognized in it

Read it in the paper: doi.org/10.1016/j.redox.2026.104127.

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, pages, dates, 9 authors, 6 keywords, 14 MeSH terms, 3 funders, 70 references.

Cite

This paper

Wang, Z., Zhou, L., Zhao, N., Li, T., Geng, F., Kong, J., Zhang, Y., Zhang, Z., & Ren, Q.-G. (2026). SLC22A3 deficiency leads to cognitive impairment through the cardio-neuroinflammatory axis mediated HA/H1R/NLRP3 pathway in heart failure mice. Redox biology, 92, 104127. https://doi.org/10.1016/j.redox.2026.104127

BibTeX

@article{wang2026slc22a3,
author = {Wang, Zhitian and Zhou, Lv and Zhao, Na and Li, Tianxiao and Geng, Fan and Kong, Jingting and Zhang, Yahao and Zhang, Zhijun and Ren, Qing-Guo},
title = {{SLC22A3 deficiency leads to cognitive impairment through the cardio-neuroinflammatory axis mediated HA/H1R/NLRP3 pathway in heart failure mice}},
journal = {Redox biology},
year = {2026},
month = mar,
volume = {92},
pages = {104127},
publisher = {Elsevier},
issn = {2213-2317},
doi = {10.1016/j.redox.2026.104127},
url = {https://doi.org/10.1016/j.redox.2026.104127},
pmid = {41833108},
pmcid = {PMC12999320}
}

RIS

TY - JOUR
AU - Wang, Zhitian
AU - Zhou, Lv
AU - Zhao, Na
AU - Li, Tianxiao
AU - Geng, Fan
AU - Kong, Jingting
AU - Zhang, Yahao
AU - Zhang, Zhijun
AU - Ren, Qing-Guo
TI - SLC22A3 deficiency leads to cognitive impairment through the cardio-neuroinflammatory axis mediated HA/H1R/NLRP3 pathway in heart failure mice
T2 - Redox biology
J2 - Redox Biol
PY - 2026
DA - 2026/03/12
VL - 92
SP - 104127
SN - 2213-2317
PB - Elsevier
DO - 10.1016/j.redox.2026.104127
UR - https://doi.org/10.1016/j.redox.2026.104127
LA - en
ER -

CSL-JSON

{
"id": "10.1016/j.redox.2026.104127",
"type": "article-journal",
"title": "SLC22A3 deficiency leads to cognitive impairment through the cardio-neuroinflammatory axis mediated HA/H1R/NLRP3 pathway in heart failure mice",
"container-title": "Redox biology",
"author": [
{
"family": "Wang",
"given": "Zhitian"
},
{
"family": "Zhou",
"given": "Lv"
},
{
"family": "Zhao",
"given": "Na"
},
{
"family": "Li",
"given": "Tianxiao"
},
{
"family": "Geng",
"given": "Fan"
},
{
"family": "Kong",
"given": "Jingting"
},
{
"family": "Zhang",
"given": "Yahao"
},
{
"family": "Zhang",
"given": "Zhijun"
},
{
"family": "Ren",
"given": "Qing-Guo"
}
],
"container-title-short": "Redox Biol",
"volume": "92",
"page": "104127",
"DOI": "10.1016/j.redox.2026.104127",
"PMID": "41833108",
"PMCID": "PMC12999320",
"ISSN": "2213-2317",
"publisher": "Elsevier",
"URL": "https://doi.org/10.1016/j.redox.2026.104127",
"language": "en",
"issued": {
"date-parts": [
[
2026,
3,
12
]
]
}
}

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/s41419-026-08862-3
O-GlcNAcylation reprograms microglial inflammatory states and attenuates Alzheimer's disease pathology.
Journal: Cell death & disease
In common: Alzheimer's / dementia, mouse, cellular / molecular, 2 references
[2] doi:10.1038/s41467-026-70694-8 [code]
Shared genetic and neuroimmune architecture links type 1 diabetes with neurocognitive traits.
Journal: Nature communications
In common: Alzheimer's / dementia, cellular / molecular, 2 references
[3] doi:10.3390/biom16060776
Alterations of Cerebral Extracellular Vesicle microRNA Profiling Potentially Disrupts Brain Homeostasis Following Myocardial Infarction.
Journal: Biomolecules
In common: cellular / molecular, 2 references
[4] doi:10.34133/csbj.0085 [code]
A Systems-Level Transcriptomic Framework Identifies Shared Cellular Hubs in Osteoarthritis and Alzheimer's Disease.
Journal: Computational and structural biotechnology journal
In common: Alzheimer's / dementia, cellular / molecular, 2 references
[5] doi:10.1007/s10565-026-10177-0
Multi-omics analysis and experimental validation reveal the IRF7-CXCL10 axis as a master regulator of microglial PCD in ischemic stroke.
Journal: Cell biology and toxicology
In common: mouse, cellular / molecular, 2 references
[6] doi:10.1097/shk.0000000000002867
Transcriptome and Experimental Verification Identified Candidate Biomarkers Related to Mitochondrial Metabolism in Sepsis-Associated Encephalopathy.
Journal: Shock (Augusta, Ga.)
In common: mouse, 2 references
[7] doi:10.1097/md.0000000000050109
The gut-immune-brain axis in CNS tumors: Causal roles of microbiota and inflammatory proteins unveiled by Mendelian randomization and single-cell transcriptomics.
Journal: Medicine
In common: cellular / molecular, 2 references
[8] doi:10.1038/s41398-026-04137-9 [code]
An integrative mendelian randomisation and drug mechanism framework for target prioritisation and therapeutic repurposing in major depression.
Journal: Translational psychiatry
In common: 2 references
[9] doi:10.1186/s12916-026-04957-y [code]
Thyroid-stimulating hormone receptor mediates peripheral-central neuroimmune crosstalk in autoimmune thyroid diseases.
Journal: BMC medicine
In common: mouse, cellular / molecular, 2 references
[10] doi:10.1038/s42003-026-10059-5 [code]
Transcriptomic analysis in autism spectrum disorder suggests three molecular subtypes with distinct phenotypic profiles and functional pathways.
Journal: Communications biology
In common: cellular / molecular, 2 references

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.

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.