Evidence map›Paper›PMID 22764104›Full record

ArticleCell death & disease2012

Mitochondrial ROS production and subsequent ERK phosphorylation are necessary for temperature preconditioning of isolated ventricular myocytes.

Y Bhagatte, D Lodwick, N Storey

Abstract read
In one paragraph

Article in Cell death & disease, 2012. 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
–field-weighted citation impact
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.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. 13-Oxyingenol dodecanoate, a cytotoxic ingenol derivative, induces mitochondrial apoptosis and caspase-dependent Akt decrease in K562 cells.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  10. Review
  11. IL-17 Induces MPTP opening through ERK2 and P53 signaling pathway in human platelets.Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban · 2015
    Article
  12. Article
  13. Article
  14. TAp73 promotes anabolism.Oncotarget · 2014
    Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. Review
  20. Protein Oxidative Modifications: Beneficial Roles in Disease and Health.Journal of biochemical and pharmacological research · 2013
    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

3 authors.

Y BhagatteDepartment of Cell Physiology and Pharmacology, College of Medicine, Biological Sciences and Psychology, University of Leicester, Leicester, UK.
D Lodwick
N Storey

Funding

British Heart Foundation FS/08/045/25508
6 · The paper itself

Abstract

Hypothermia and hypothermic preconditioning are known to be profoundly cardioprotective, but the molecular mechanisms of this protection have not been fully explained. In this study, temperature preconditioning (16 °C) was found to be cardioprotective in isolated adult rat ventricular myocytes, enhancing contractile recovery and preventing calcium dysregulation after oxidative stress. Hypothermic preconditioning preserved mitochondrial function by delaying the pathological opening of the mitochondrial permeability transition pore (mPTP), whereas transient mPTP flickering remained unaltered. For the first time, reactive oxygen species (ROS) from the mitochondria are shown to be released exclusively during the hypothermic episodes of the temperature-preconditioning protocol. Using a mitochondrially targeted ROS biosensor, ROS release was shown during the brief bursts to 16 °C of temperature preconditioning. The ROS scavenger N-(2-mercaptopropionyl) glycine attenuated ROS accumulation during temperature preconditioning, abolishing the protective delay in mPTP opening. Temperature preconditioning induces ROS-dependant phosphorylation of the prosurvival kinase extracellular signal-regulated kinase (ERK)1/2. ERK1/2 activation was shown to be downstream of ROS release, as the presence of a ROS scavenger during temperature preconditioning completely blocked ERK1/2 activation. The cardioprotective effects of temperature preconditioning on mPTP opening were completely lost by inhibiting ERK1/2 activation. Thus, mitochondrial ROS release and ERK1/2 activation are both necessary to signal the cardioprotective effects of temperature preconditioning in cardiac myocytes.

Indexed as

AnimalsCells, CulturedDisease Models, AnimalExtracellular Signal-Regulated MAP KinasesFree Radical ScavengersGlycineMaleMitochondriaMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Myocytes, CardiacPhosphorylationRatsRats, WistarExtracellular Signal-Regulated MAP KinasesFree Radical ScavengersGlycineMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3N-(2-mercaptoproprionyl)-glycineReactive Oxygen SpeciesSulfhydryl Compounds

Identifiers

PMID22764104
PMCPMC3406583

What OpenQuestion holds

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LicenceCC BY-NC-ND
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Registered trials

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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.