Evidence map›Paper›PMID 27381825›Full record

ArticleJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism2017

Sestrin2, as a negative feedback regulator of mTOR, provides neuroprotection by activation AMPK phosphorylation in neonatal hypoxic-ischemic encephalopathy in rat pups.

Xudan Shi, Liang Xu, Desislava Met Doycheva, Jiping Tang, Min Yan, John H Zhang

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
7.2field-weighted citation impact, top 2% 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

42 citing papers in PubMed, 81 citations in OpenAlex.

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  15. Sestrin2 in hypoxia and hypoxia-related diseases.Redox report : communications in free radical research · 2021
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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 2 institutions in 2 countries.

Xudan Shi1 Department of Anesthesiology, School of Medicine, The Second Affiliated Hospital, Zhejiang University, Hangzhou, Zhejiang, China.
Liang Xu2 Departments of Anesthesiology and Basic Sciences, School of Medicine, Loma Linda University, Loma Linda, CA, USA.
Desislava Met Doycheva2 Departments of Anesthesiology and Basic Sciences, School of Medicine, Loma Linda University, Loma Linda, CA, USA.
Jiping Tang2 Departments of Anesthesiology and Basic Sciences, School of Medicine, Loma Linda University, Loma Linda, CA, USA.
Min Yan1 Department of Anesthesiology, School of Medicine, The Second Affiliated Hospital, Zhejiang University, Hangzhou, Zhejiang, China.
John H Zhang2 Departments of Anesthesiology and Basic Sciences, School of Medicine, Loma Linda University, Loma Linda, CA, USA.
Loma Linda University · USSecond Affiliated Hospital of Zhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hypoxic-ischemic encephalopathy is a condition caused by reduced oxygen and cerebral blood flow to the brain resulting in neurological impairments. Effective therapeutic treatments to ameliorate these disabilities are still lacking. We sought to investigate the role of sestrin2, a highly conserved stress-inducible protein, in a neonatal rat hypoxic-ischemic encephalopathy model. Ten-day-old rat pups underwent right common carotid artery ligation followed by 2.5 h hypoxia. At 1 h post hypoxic-ischemic encephalopathy, rats were intranasally administered with recombinant human sestrin2 and sacrificed for brain infarct area measurement, Fluoro-Jade C, immunofluorescence staining, Western blot, and neurological function testing. rh-sestrin2 reduced brain infarct area, brain atrophy, apoptosis, ventricular area enlargement, and improved neurological function. Western blot showed that sestrin2 expression levels were increased after treatment with rh-sestrin2, and sestrin2 exerts neuroprotective effects via activation of the adenosine monophosphate-activated protein kinase pathway which in turn inhibits mammalian target of rapamycin signaling resulting in the attenuation of apoptosis. In conclusions: Sestrin2 plays an important neuroprotective role after hypoxic-ischemic encephalopathy via adenosine monophosphate-activated protein kinase signaling pathway and serves as a negative feedback regulator of mammalian target of rapamycin. Administration of rh-sestrin2 not only reduced infarct area and brain atrophy, but also significantly improved neurological function.

Indexed as

AMP-Activated Protein KinasesAnimalsAnimals, NewbornBehavior, AnimalBlotting, WesternBrainFeedback, PhysiologicalHypoxia-Ischemia, BrainNeuroprotective AgentsNuclear ProteinsPhosphorylationRats, Sprague-DawleyRecombinant ProteinsRNA, Small InterferingSestrinsSignal TransductionAMP-Activated Protein KinasesmTOR protein, ratNeuroprotective AgentsNuclear ProteinsRecombinant ProteinsRNA, Small InterferingSESN2 protein, humanSesn2 protein, ratSestrinsTOR Serine-Threonine Kinasesadenosine monophosphate-activated protein kinaseapoptosismammalian target of rapamycinneonatal hypoxic-ischemic encephalopathySestrins

Identifiers

PMID27381825
PMCPMC5453464
OpenAlexW2468097483

What OpenQuestion 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 OpenQuestion graph.