Evidence map›Paper›PMID 26840743›Full record

ArticlePloS one2016

Urocortin-1 Mediated Cardioprotection Involves XIAP and CD40-Ligand Recovery: Role of EPAC2 and ERK1/2.

Eva Calderón-Sánchez, Ignacio Díaz, Antonio Ordóñez, Tarik Smani

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.0field-weighted citation impact, top 16% 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

15 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Review
  10. Epac Function and cAMP Scaffolds in the Heart and Lung.Journal of cardiovascular development and disease · 2018
    Review
  11. Urocortin-2 Prevents Dysregulation of CaFrontiers in physiology · 2018
    Article
  12. Article
  13. Article
  14. Article
  15. 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

4 authors at 2 institutions in 1 country.

Eva Calderón-SánchezGrupo de Fisiopatología Cardiovascular, Instituto de Biomedicina de Sevilla-IBiS, HUVR/Universidad de Sevilla/CSIC, Seville, Spain.
Ignacio DíazGrupo de Fisiopatología Cardiovascular, Instituto de Biomedicina de Sevilla-IBiS, HUVR/Universidad de Sevilla/CSIC, Seville, Spain.
Antonio OrdóñezGrupo de Fisiopatología Cardiovascular, Instituto de Biomedicina de Sevilla-IBiS, HUVR/Universidad de Sevilla/CSIC, Seville, Spain.
Tarik SmaniGrupo de Fisiopatología Cardiovascular, Instituto de Biomedicina de Sevilla-IBiS, HUVR/Universidad de Sevilla/CSIC, Seville, Spain.
Instituto de Biomedicina de Sevilla · ESUniversidad de Sevilla · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsUrocortin-1 (Ucn-1) is an endogenous peptide that protects heart from ischemia and reperfusion (I/R) injuries. Ucn-1 is known to prevent cardiac cell death, but its role in the transcription of specific genes related to survival signaling pathway has not been fully defined. The aim of this study was to investigate the molecular signaling implicated in the improvement of cardiac myocytes survival induced by Ucn-1. METHODS AND

resultsUcn-1 administration before ischemia and at the onset of reperfusion, in rat hearts perfused in Langendorff system, fully recovered heart contractility and other hemodynamic parameters. Ucn-1 enhanced cell viability and decreased lactate dehydrogenase (LDH) release in adult cardiac myocytes subjected to simulated I/R. Annexin V-FITC/PI staining indicated that Ucn-1 promoted cell survival and decreased cell necrosis through Epac2 (exchange protein directly activated by cAMP) and ERK1/2 (extracellular signal-regulated kinases 1/2) activation. We determined that Ucn-1 shifted cell death from necrosis to apoptosis and activated caspases 9 and 3/7. Furthermore, mini-array, RT-qPCR and protein analyses of apoptotic genes showed that Ucn-1 upregulated the expression of CD40lg, Xiap and BAD in cells undergoing I/R, involving Epac2 and ERK1/2 activation.

conclusionsOur data indicate that Ucn-1 efficiently protected hearts from I/R damage by increasing the cell survival and stimulated apoptotic genes, CD40lg, Xiap and BAD, overexpression through the activation of Epac2 and ERK1/2.

Indexed as

AnimalsApoptosisCardiotonic AgentsCaspasesCD40 LigandCell SurvivalDisease Models, AnimalGene Expression RegulationGuanine Nucleotide Exchange FactorsHemodynamicsMaleMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Myocardial ContractionMyocardial Reperfusion InjuryMyocardiumCardiotonic AgentsCaspasesCD40 LigandGuanine Nucleotide Exchange FactorsMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Rapgef4 protein, ratUrocortinsX-Linked Inhibitor of Apoptosis Protein

Identifiers

PMID26840743
PMCPMC4739601
OpenAlexW2263785644

What OpenQuestion holds

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LicenceCC BY
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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.