Evidence map›Paper›PMID 29921218›Full record

ArticleBMC cell biology2018

A comparison of LKB1/AMPK/mTOR metabolic axis response to global ischaemia in brain, heart, liver and kidney in a rat model of cardiac arrest.

Shohreh Majd, John H T Power, Timothy K Chataway, Hugh J M Grantham

Open access · goldAbstract readComparative Study
In one paragraph

Article in BMC cell biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

20 citing papers in PubMed, 30 citations in OpenAlex.

  1. Mechanism of post cardiac arrest syndrome based on animal models of cardiac arrest.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2025
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  12. Mitochondria-localized AMPK responds to local energetics and contributes to exercise and energetic stress-induced mitophagy.Proceedings of the National Academy of Sciences of the United States of America · 2021
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  13. Article
  14. Activation of AMPK under Hypoxia: Many Roads Leading to Rome.International journal of molecular sciences · 2020
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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

4 authors at 1 institution in 1 country.

Shohreh MajdCentre for Neuroscience, Neuronal Injury and Repair Laboratory, College of Medicine and Health Sciences, Flinders University, Adelaide, SA, 5042, Australia. shohreh.majd@flinders.edu.au.ORCID 0000-0002-7051-2090
John H T PowerCentre for Neuroscience, Neuronal Injury and Repair Laboratory, College of Medicine and Public Health, Flinders University of South Australia, Adelaide, SA, 5042, Australia.
Timothy K ChatawayProteomics Facility, College of Medicine and Public Health, Flinders University, Adelaide, SA, 5042, Australia.
Hugh J M GranthamCentre for Neuroscience, Neuronal Injury and Repair Laboratory, College of Medicine and Public Health, Flinders University of South Australia, Adelaide, SA, 5042, Australia.
Flinders University · AU

Funding

Australian Resuscitation Council RPF13/771Flinders University 39468
6 · The paper itself

Abstract

backgroundCellular energy failure in high metabolic rate organs is one of the underlying causes for many disorders such as neurodegenerative diseases, cardiomyopathies, liver and renal failures. In the past decade, numerous studies have discovered the cellular axis of LKB1/AMPK/mTOR as an essential modulator of cell homeostasis in response to energy stress. Through regulating adaptive mechanisms, this axis adjusts the energy availability to its demand by a systematized control on metabolism. Energy stress, however, could be sensed at different levels in various tissues, leading to applying different strategies in response to hypoxic insults.

methodsHere the immediate strategies of high metabolic rate organs to time-dependent short episodes of ischaemia were studied by using a rat model (n = 6/group) of cardiac arrest (CA) (15 and 30 s, 1, 2, 4 and 8 min CA). Using western blot analysis, we examined the responses of LKB1/AMPK/mTOR pathway in brain, heart, liver and kidney from 15 s up to 8 min of global ischaemia. The ratio of ADP/ATP was assessed in all ischemic and control groups, using ApoSENSOR bioluminescent assay kit.

resultsBrain, followed by kidney showed the early dephosphorylation response in AMPK (Thr

conclusionTogether our results suggest that early AMPK dephosphorylation followed by late hyperphosphorylation is the strategy of brain and kidney in response to ischaemia. While the liver seemed to get benefit of its AMPK system in early ischameia, possibly to stabilize ATP, the level of LKB1/AMPK activity in heart remained unchanged in short ischaemic episodes up to 8 min. Further researches must be conducted to elucidate the molecular mechanism underlying LKB1/AMPK response to oxygen supply.

Indexed as

Organ SpecificitySignal TransductionAdenosine DiphosphateAdenosine TriphosphateAMP-Activated Protein Kinase KinasesAMP-Activated Protein KinasesAnimalsBrainDisease Models, AnimalElectrocardiographyHeart ArrestIschemiaKidneyLiverMyocardiumPhosphorylationAdenosine DiphosphateAdenosine TriphosphateAMP-Activated Protein Kinase KinasesAMP-Activated Protein KinasesProtein Serine-Threonine KinasesStk11 protein, ratTOR Serine-Threonine KinasesAdenosine monophosphate kinase protein kinaseADP/ATPAMPKBioluminescent assayBrainCardiac arrestCell energy stressHeartIschaemiaKidneyLiverLiver kinase b1LKBMammalian target of rapamycinmTORSprague Dawley ratWestern blot

Identifiers

PMID29921218
PMCPMC6010165
OpenAlexW2809531901

What OpenQuestion 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 OpenQuestion graph.