Evidence map›Paper›PMID 24155931›Full record

ArticlePloS one2013

Apolipoprotein a-I is a potential mediator of remote ischemic preconditioning.

Pierre Hibert, Delphine Prunier-Mirebeau, Olivia Beseme, Maggy Chwastyniak, Sophie Tamareille, Delphine Lamon, Alain Furber, Florence Pinet, Fabrice Prunier

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
5.8field-weighted citation impact, top 4% 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

31 citing papers in PubMed, 1 synthesis or guideline pooled it, 53 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Article
  5. Article
  6. Review
  7. Perioperative Cardioprotection by Remote Ischemic Conditioning.International journal of molecular sciences · 2019
    Review
  8. Review
  9. Review
  10. Correction to: Neuroimmune Response in Ischemic Preconditioning.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2018
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Cardioprotection by remote ischemic conditioning and its signal transduction.Pflugers Archiv : European journal of physiology · 2017
    Review
  17. Article
  18. Article
  19. Neuroimmune Response in Ischemic Preconditioning.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2016
    Review
  20. 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

9 authors at 5 institutions in 1 country.

Pierre HibertL'UNAM Université, Angers, France ; Laboratoire Cardioprotection, Remodelage et Thrombose, Université d'Angers, Angers, France.
Delphine Prunier-Mirebeau
Olivia Beseme
Maggy Chwastyniak
Sophie Tamareille
Delphine Lamon
Alain Furber
Florence Pinet
Fabrice Prunier
Université d'Angers · FRInstitut Pasteur de Lille · FRCentre National de la Recherche Scientifique · FRInserm · FRUniversité Nantes Angers Le Mans · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundRemote ischemic preconditioning (RIPC) has emerged as an attractive strategy in clinical settings. Despite convincing evidence of the critical role played by circulating humoral mediators, their actual identities remain unknown. In this study, we aimed to identify RIPC-induced humoral mediators using a proteomic approach.

methodsand Results Rats were exposed to 10-min limb ischemia followed by 5- (RIPC 5') or 10-min (RIPC 10') reperfusion prior to blood sampling. The control group only underwent blood sampling. Plasma samples were analyzed using surface-enhanced laser desorption and ionization - time of flight - mass spectrometry (SELDI-TOF-MS). Three protein peaks were selected for their significant increase in RIPC 10'. They were identified and confirmed as apolipoprotein A-I (ApoA-I). Additional rats were exposed to myocardial ischemia-reperfusion (I/R) and assigned to one of the following groups RIPC+myocardial infarction (MI) (10-min limb ischemia followed by 10-min reperfusion initiated 20 minutes prior to myocardial I/R), ApoA-I+MI (10 mg/kg ApoA-I injection 10 minutes before myocardial I/R), and MI (no further intervention). In comparison with untreated MI rats, RIPC reduced infarct size (52.2±3.7% in RIPC+MI vs. 64.9±2.6% in MI; p<0.05). Similarly, ApoA-I injection decreased infarct size (50.9±3.8%; p<0.05 vs. MI).

conclusionsRIPC was associated with a plasmatic increase in ApoA-I. Furthermore, ApoA-I injection before myocardial I/R recapitulated the cardioprotection offered by RIPC in rats. This data suggests that ApoA-I may be a protective blood-borne factor involved in the RIPC mechanism.

Indexed as

Ischemic PreconditioningAnimalsApolipoprotein A-ICardiotonic AgentsEnzyme-Linked Immunosorbent AssayMaleMyocardial Reperfusion InjuryProteomicsRatsRats, WistarReproducibility of ResultsSpectrometry, Mass, Matrix-Assisted Laser Desorption-IonizationApolipoprotein A-ICardiotonic Agents

Identifiers

PMID24155931
PMCPMC3796499
OpenAlexW2006391524

What OpenQuestion holds

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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.