Evidence map›Paper›PMID 37516843›Full record

ArticleJournal of neuroinflammation2023

Targeted ablation of signal transducer and activator of transduction 1 alleviates inflammation by microglia/macrophages and promotes long-term recovery after ischemic stroke.

Wenxuan Han, Hongjian Pu, Sicheng Li, Yaan Liu, Yongfang Zhao, Mingyue Xu, Caixia Chen, Yun Wu, Tuo Yang, Qing Ye and 4 more

Open access · goldAbstract read
In one paragraph

Article in Journal of neuroinflammation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 11% 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

12 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Monocyte-derived macrophages and their roles in ischemic stroke.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2026
    Review
  6. Targeting angiogenesis and white matter repair for enhanced functional recovery after acute ischemic stroke: A focus on the roles of glial cells.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2026
    Review
  7. Article
  8. Article
  9. Review
  10. Review
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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 1 institution in 1 country.

Wenxuan Han *Pittsburgh Institute of Brain Disorders and Recovery and Department of Neurology, University of Pittsburgh, 3500 Terrace Street, S-510 BST, Pittsburgh, PA, 15213, USA.
Hongjian Pu *Pittsburgh Institute of Brain Disorders and Recovery and Department of Neurology, University of Pittsburgh, 3500 Terrace Street, S-510 BST, Pittsburgh, PA, 15213, USA.
Sicheng LiPittsburgh Institute of Brain Disorders and Recovery and Department of Neurology, University of Pittsburgh, 3500 Terrace Street, S-510 BST, Pittsburgh, PA, 15213, USA.
Yaan LiuPittsburgh Institute of Brain Disorders and Recovery and Department of Neurology, University of Pittsburgh, 3500 Terrace Street, S-510 BST, Pittsburgh, PA, 15213, USA.
Yongfang ZhaoPittsburgh Institute of Brain Disorders and Recovery and Department of Neurology, University of Pittsburgh, 3500 Terrace Street, S-510 BST, Pittsburgh, PA, 15213, USA.
Mingyue XuPittsburgh Institute of Brain Disorders and Recovery and Department of Neurology, University of Pittsburgh, 3500 Terrace Street, S-510 BST, Pittsburgh, PA, 15213, USA.
Caixia ChenPittsburgh Institute of Brain Disorders and Recovery and Department of Neurology, University of Pittsburgh, 3500 Terrace Street, S-510 BST, Pittsburgh, PA, 15213, USA.
Yun WuPittsburgh Institute of Brain Disorders and Recovery and Department of Neurology, University of Pittsburgh, 3500 Terrace Street, S-510 BST, Pittsburgh, PA, 15213, USA.
Tuo YangPittsburgh Institute of Brain Disorders and Recovery and Department of Neurology, University of Pittsburgh, 3500 Terrace Street, S-510 BST, Pittsburgh, PA, 15213, USA.
Qing YePittsburgh Institute of Brain Disorders and Recovery and Department of Neurology, University of Pittsburgh, 3500 Terrace Street, S-510 BST, Pittsburgh, PA, 15213, USA.
Hong WangDepartment of Biostatistics, University of Pittsburgh, Pittsburgh, PA, 15213, USA.
R Anne StetlerPittsburgh Institute of Brain Disorders and Recovery and Department of Neurology, University of Pittsburgh, 3500 Terrace Street, S-510 BST, Pittsburgh, PA, 15213, USA.
Jun ChenPittsburgh Institute of Brain Disorders and Recovery and Department of Neurology, University of Pittsburgh, 3500 Terrace Street, S-510 BST, Pittsburgh, PA, 15213, USA.
Yejie ShiPittsburgh Institute of Brain Disorders and Recovery and Department of Neurology, University of Pittsburgh, 3500 Terrace Street, S-510 BST, Pittsburgh, PA, 15213, USA. y.shi@pitt.edu.
University of Pittsburgh · US

Funding

Modulating microglia and macrophage functions to promote stroke recoveryR01NS117550 · NINDS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI SHI, YEJIE · 2021 to 2025
$2.0M
BLRD Research Career Scientist Award ApplicationIK6BX006298 · VA · VETERANS HEALTH ADMINISTRATION · PI CHEN, JUN · 2023 to 2025
–
BLRD VA I01 BX003377BLRD VA IK6 BX006298NIH HHS R01 NS117550NINDS NIH HHS R01 NS117550
6 · The paper itself

Abstract

backgroundBrain microglia and macrophages (Mi/MΦ) can shift to a harmful or advantageous phenotype following an ischemic stroke. Identification of key molecules that regulate the transformation of resting Mi/MΦ could aid in the development of innovative therapies for ischemic stroke. The transcription factor signal transducer and activator of transduction 1 (STAT1) has been found to contribute to acute neuronal death (in the first 24 h) following ischemic stroke, but its effects on Mi/MΦ and influence on long-term stroke outcomes have yet to be determined.

methodsWe generated mice with tamoxifen-induced, Mi/MΦ-specific knockout (mKO) of STAT1 driven by Cx3cr1

resultsSTAT1 was activated in Mi/MΦ at the subacute stage (3 days) after MCAO. Selective deletion of STAT1 in Mi/MΦ did not alter neuronal cell death or infarct size at 24 h after MCAO, but attenuated Mi/MΦ release of high mobility group box 1 and increased arginase 1-producing Mi/MΦ 3d after MCAO, suggesting boosted inflammation-resolving responses of Mi/MΦ. As a result, STAT1 mKO mice had mitigated brain inflammation at the subacute stage after MCAO and less white matter injury in the long term. Importantly, STAT1 mKO was sufficient to improve functional recovery for at least 5 weeks after MCAO in both male and female mice.

conclusionsMi/MΦ-targeted STAT1 KO does not provide immediate neuroprotection but augments inflammation-resolving actions of Mi/MΦ, thereby facilitating long-term functional recovery after stroke. STAT1 is, therefore, a promising therapeutic target to harness beneficial Mi/MΦ responses and improve long-term outcomes after ischemic stroke.

Indexed as

EncephalitisIschemic StrokeStrokeAnimalsFemaleInflammationMacrophagesMaleMiceMicrogliaSTAT1 Transcription FactorStat1 protein, mouseSTAT1 Transcription FactorBehavior testConditional gene knockoutNeuroinflammationSTAT1White matter injury

Identifiers

PMID37516843
PMCPMC10385956
OpenAlexW4385380158

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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 OpenQuestion graph.