Evidence map›Paper›PMID 32363721›Full record

ArticleJournal of cellular and molecular medicine2020

Sestrin 2 attenuates sepsis-associated encephalopathy through the promotion of autophagy in hippocampal neurons.

Lili Luo, Jinlin Wu, Lina Qiao, Guoyan Lu, Jinhui Li, Deyuan Li

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.6field-weighted citation impact, top 9% 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

21 citing papers in PubMed, 32 citations in OpenAlex.

  1. Research Advances in the Pathogenesis of Sepsis-Associated Encephalopathy.International journal of molecular sciences · 2026
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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

6 authors at 1 institution in 1 country.

Lili LuoDepartment of Pediatrics, West China Second University Hospital, Sichuan University, Chengdu, China.
Jinlin WuDepartment of Pediatrics, West China Second University Hospital, Sichuan University, Chengdu, China.
Lina QiaoDepartment of Pediatrics, West China Second University Hospital, Sichuan University, Chengdu, China.
Guoyan LuDepartment of Pediatrics, West China Second University Hospital, Sichuan University, Chengdu, China.
Jinhui LiDepartment of Pediatrics, West China Second University Hospital, Sichuan University, Chengdu, China.
Deyuan LiDepartment of Pediatrics, West China Second University Hospital, Sichuan University, Chengdu, China.ORCID 0000-0003-3746-1110
Ministry of Education of the People's Republic of China · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sepsis-associated encephalopathy (SAE) has typically been associated with a poor prognosis. Although sestrin 2 (SESN2) plays a crucial role in metabolic regulation and the stress response, its expression and functional roles in SAE are still unclear. In the present study, SAE was established in mice through caecal ligation and puncture (CLP). The adeno-associated virus 2 (AAV2)-mediated SESN2 expression (ie overexpression and knockdown) system was injected into the hippocampi of mice with SAE, and subsequently followed by electron microscopic analysis, the Morris water maze task and pathological examination. Our results demonstrated an increase of SESN2 in the hippocampal neurons of mice with SAE, 2-16 hours following CLP. AAV2-mediated ectopic expression of SESN2 attenuated brain damage and loss of learning and memory functions in mice with SAE, and these effects were associated with lower pro-inflammatory cytokines in the hippocampus. Mechanistically, SESN2 promoted unc-51-like kinase 1 (ULK1)-dependent autophagy in hippocampal neurons through the activation of the AMPK/mTOR signalling pathway. Finally, AMPK inhibition by SBI-0206965 blocked SESN2-mediated attenuation of SAE in mice. In conclusion, our findings demonstrated that SESN2 might be a novel pharmacological intervention strategy for SAE treatment through promotion of ULK1-dependent autophagy in hippocampal neurons.

Indexed as

AutophagyAdenylate KinaseAnimalsAutophagosomesAutophagy-Related Protein-1 HomologFemaleHippocampusMice, Inbred C57BLNeuronsPeroxidasesSepsis-Associated EncephalopathySestrinsSignal TransductionTOR Serine-Threonine KinasesUp-RegulationAdenylate KinaseAutophagy-Related Protein-1 HomologPeroxidasesSesn2 protein, mouseSestrinsTOR Serine-Threonine Kinasesautophagysepsis-associated encephalopathySESN2unc-51-like kinase 1

Identifiers

PMID32363721
PMCPMC7299720
OpenAlexW3023787735

What Socratic holds

Textmetadata
LicenceCC BY
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.