Evidence map›Paper›PMID 42310721›Full record

ArticleCell communication and signaling : CCS2026

Paraventricular oxytocin neurons attenuate post-ischemic brain injury by suppressing microglia-mediated neuroinflammation.

Rui Liu, Xinyu Yang, Haozhi Gong, Huijie Fang, Xuebing Feng, Jiayao Li, Wentao Gao, Xiaoting Liang, Yanping Shen, Yubo Wang and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell communication and signaling : CCS, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

13 authors.

Rui Liu *Department of Neurosurgery and Department of Interventional Radiology, Xuanwu Hospital, Capital Medical University, Beijing, China.
Xinyu Yang *Department of Neurosurgery and Department of Interventional Radiology, Xuanwu Hospital, Capital Medical University, Beijing, China.
Haozhi GongDepartment of Neurosurgery and Department of Interventional Radiology, Xuanwu Hospital, Capital Medical University, Beijing, China.
Huijie FangDepartment of Neurosurgery and Department of Interventional Radiology, Xuanwu Hospital, Capital Medical University, Beijing, China.
Xuebing FengDepartment of Neurosurgery and Department of Interventional Radiology, Xuanwu Hospital, Capital Medical University, Beijing, China.
Jiayao LiDepartment of Neurosurgery and Department of Interventional Radiology, Xuanwu Hospital, Capital Medical University, Beijing, China.
Wentao GaoDepartment of Neurosurgery and Department of Interventional Radiology, Xuanwu Hospital, Capital Medical University, Beijing, China.
Xiaoting LiangDepartment of Neurosurgery and Department of Interventional Radiology, Xuanwu Hospital, Capital Medical University, Beijing, China.
Yanping ShenDepartment of Neurosurgery and Department of Interventional Radiology, Xuanwu Hospital, Capital Medical University, Beijing, China.
Yubo WangDepartment of Neurosurgery and Department of Interventional Radiology, Xuanwu Hospital, Capital Medical University, Beijing, China.
Wei WangDepartment of Neurology, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, China. ndyfy07808@ncu.edu.cn.
Jiaqi JinDepartment of Neurosurgery and Department of Interventional Radiology, Xuanwu Hospital, Capital Medical University, Beijing, China. jinjiaqi@xwhosp.org.
Liqun JiaoDepartment of Neurosurgery and Department of Interventional Radiology, Xuanwu Hospital, Capital Medical University, Beijing, China. liqunjiao@sina.cn.

Funding

the Beijing Natural Science Foundation L252081the Capital Medical Science Innovation Center Organized Research Special Program CX25YZ05the National Natural Science Foundation of China 8240051347
6 · The paper itself

Abstract

backgroundNeuroinflammation is caused by the overactivation of microglia, contributing to secondary brain injury in ischemic stroke. Oxytocin (OXT), a neuropeptide synthesized by neurons in the paraventricular nucleus (PVN) of the hypothalamus, has demonstrated potential in mitigating inflammatory responses across various pathological conditions. However, research on the role of PVN

methodsTransient middle cerebral artery occlusion (tMCAO) was performed in mice. OXT levels were measured in the peri-infarct cortex, serum, and cerebrospinal fluid (CSF), and OXTR expression was assessed in the peri-infarct cortex after tMCAO. Chemogenetic approaches were used to selectively activate PVN

resultsOXT levels significantly reduced in the peri-infarct cortex, serum, and CSF, whereas OXTR expression increased in the peri-infarct cortex after tMCAO. Chemogenetic activation of PVN

conclusionsPVN

Indexed as

Brain IschemiaMicrogliaNeuroinflammatory DiseasesNeuronsOxytocinParaventricular Hypothalamic NucleusAnimalsInfarction, Middle Cerebral ArteryMaleMiceMice, Inbred C57BLReceptors, OxytocinOxytocinReceptors, OxytocinIschemic strokeMicrogliaNeutrophil chemotaxisOxytocinParaventricular nucleus

Identifiers

PMID42310721
PMCPMC13508365

What Socratic holds

Textmetadata
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.