Evidence map›Paper›PMID 37488863›Full record

ArticleNeural regeneration research2024

Spi1 regulates the microglial/macrophage inflammatory response via the PI3K/AKT/mTOR signaling pathway after intracerebral hemorrhage.

Guoqiang Zhang, Jianan Lu, Jingwei Zheng, Shuhao Mei, Huaming Li, Xiaotao Zhang, An Ping, Shiqi Gao, Yuanjian Fang, Jun Yu

Open access · goldAbstract read
In one paragraph

Article in Neural regeneration research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
10.7field-weighted citation impact, top 1% 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

39 citing papers in PubMed, 52 citations in OpenAlex.

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  8. PU.1: the conductor of Alzheimer's symphony.Molecular neurodegeneration · 2026
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  20. S-Ketamine Alleviates Anxiety-Induced Chronic Postoperative Pain by Affecting Glucose Metabolism of Striatal Microglia in a Rat Model.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025
    Article
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

10 authors at 2 institutions in 1 country.

Guoqiang ZhangDepartment of Neurosurgery, The Second Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou, Zhejiang Province, China.
Jianan LuDepartment of Neurosurgery, The Second Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou, Zhejiang Province, China.
Jingwei ZhengDepartment of Neurosurgery, The Second Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou, Zhejiang Province, China.
Shuhao MeiDepartment of Neurosurgery, Huashan Hospital of Fudan University School of Medicine, Shanghai, China.
Huaming LiDepartment of Neurosurgery, The Second Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou, Zhejiang Province, China.
Xiaotao ZhangDepartment of Neurosurgery, The Second Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou, Zhejiang Province, China.
An PingDepartment of Neurosurgery, The Second Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou, Zhejiang Province, China.
Shiqi GaoDepartment of Neurosurgery, The Second Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou, Zhejiang Province, China.
Yuanjian FangDepartment of Neurosurgery, The Second Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou, Zhejiang Province, China.
Jun YuDepartment of Neurosurgery, The Second Affiliated Hospital of Zhejiang University School of Medicine; Clinical Research Center for Neurological Diseases of Zhejiang Province; Key Laboratory of Precise Treatment and Clinical Translational Research of Neurological Diseases, Hangzhou, Zhejiang Province, China.
Second Affiliated Hospital of Zhejiang University · CNFudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Preclinical and clinical studies have shown that microglia and macrophages participate in a multiphasic brain damage repair process following intracerebral hemorrhage. The E26 transformation-specific sequence-related transcription factor Spi1 regulates microglial/macrophage commitment and maturation. However, the effect of Spi1 on intracerebral hemorrhage remains unclear. In this study, we found that Spi1 may regulate recovery from the neuroinflammation and neurofunctional damage caused by intracerebral hemorrhage by modulating the microglial/macrophage transcriptome. We showed that high Spi1 expression in microglia/macrophages after intracerebral hemorrhage is associated with the activation of many pathways that promote phagocytosis, glycolysis, and autophagy, as well as debris clearance and sustained remyelination. Notably, microglia with higher levels of Spi1 expression were characterized by activation of pathways associated with a variety of hemorrhage-related cellular processes, such as complement activation, angiogenesis, and coagulation. In conclusion, our results suggest that Spi1 plays a vital role in the microglial/macrophage inflammatory response following intracerebral hemorrhage. This new insight into the regulation of Spi1 and its target genes may advance our understanding of neuroinflammation in intracerebral hemorrhage and provide therapeutic targets for patients with intracerebral hemorrhage.

Indexed as

intracerebral hemorrhagemacrophagemicroglianeuroinflammationphagocytosisPI3K/AKT/mTOR signaling pathwaySpi1transcriptomics

Identifiers

PMID37488863
PMCPMC10479839
OpenAlexW4378218338

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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 OpenQuestion graph.