Evidence map›Paper›PMID 31612615›Full record

ArticleCNS neuroscience & therapeutics2020

Regulation of hippocampal neuronal apoptosis and autophagy in mice with sepsis-associated encephalopathy by immunity-related GTPase M1.

Rui-Xi Zhou, Yu-Yao Li, Yi Qu, Qun Huang, Xue-Mei Sun, De-Zhi Mu, Xi-Hong Li

Open access · goldAbstract read
In one paragraph

Article in CNS neuroscience & therapeutics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

29 citing papers in PubMed, 38 citations in OpenAlex.

  1. Review
  2. Research Advances in the Pathogenesis of Sepsis-Associated Encephalopathy.International journal of molecular sciences · 2026
    Review
  3. Article
  4. Article
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  8. Review
  9. Article
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  16. AQP4 Aggravates Cognitive Impairment in Sepsis-Associated Encephalopathy through Inhibiting NaAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023
    Article
  17. Review
  18. Review
  19. lncRNA Neat1 regulates neuronal dysfunction post-sepsis via stabilization of hemoglobin subunit beta.Molecular therapy : the journal of the American Society of Gene Therapy · 2022
    Article
  20. Review
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

7 authors at 2 institutions in 1 country.

Rui-Xi ZhouDepartment of Pediatrics, West China Second University Hospital, Sichuan University, Chengdu, China.
Yu-Yao LiClinical Medical College, Xiamen University, Xiamen, China.
Yi QuDepartment of Pediatrics, West China Second University Hospital, Sichuan University, Chengdu, China.ORCID 0000-0002-9993-8810
Qun HuangDepartment of Pediatrics, West China Second University Hospital, Sichuan University, Chengdu, China.
Xue-Mei SunDepartment of Pediatrics, West China Second University Hospital, Sichuan University, Chengdu, China.
De-Zhi MuDepartment of Pediatrics, West China Second University Hospital, Sichuan University, Chengdu, China.
Xi-Hong LiDepartment of Pediatrics, West China Second University Hospital, Sichuan University, Chengdu, China.ORCID 0000-0001-7937-2875
Sichuan University · CNXiamen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsSepsis-associated encephalopathy (SAE) is a common complication of severe sepsis. Our goal was to investigate the role of immunity-related GTPase M1 (IRGM1) in SAE and its underlying mechanism.

methodsA mouse sepsis model was established by cecal ligation and perforation. SAE was diagnosed by behavior, electroencephalography, and somatosensory evoked potentials. Wild-type mice with SAE were treated with SB203580 to block the p38 mitogen-activated protein kinase (MAPK) signaling pathway. We assessed hippocampal histological changes and the expression of IRGM1, interferon-γ (IFN-γ), and p38 MAPK signaling pathway-related proteins.

resultsImmunity-related GTPase M1 and IFN-γ levels increased in the hippocampus, with apoptosis, autophagy, and the p38 MAPK signaling pathway activated in neurons. Administration of SB203580 to mice with SAE reduced apoptosis and autophagy. Relative to wild-type mice with SAE, the general condition of Irgm1

conclusionsDuring SAE, IRGM1 can at least partially regulate apoptosis and autophagy in hippocampal neurons through the p38 MAPK signaling pathway.

Indexed as

ApoptosisAnimalsBehavior, AnimalElectroencephalographyEvoked Potentials, SomatosensoryGTP-Binding ProteinsHippocampusImidazolesInterferon-gammaIntestinal PerforationMaleMiceMice, Inbred C57BLMice, KnockoutNeuronsp38 Mitogen-Activated Protein KinasesGTP-Binding ProteinsIfi1 protein, mouseImidazolesInterferon-gammap38 Mitogen-Activated Protein KinasesPyridinesSB 203580apoptosisautophagyimmunity-related GTPase M1p38 mitogen-activated protein kinasesepsis-related encephalopathy

Identifiers

PMID31612615
PMCPMC6978258
OpenAlexW2980453994

What OpenQuestion holds

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LicenceCC BY
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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.