Evidence map›Paper›PMID 26161239›Full record

ArticleOxidative medicine and cellular longevity2015

Adenosine 2B Receptor Activation Reduces Myocardial Reperfusion Injury by Promoting Anti-Inflammatory Macrophages Differentiation via PI3K/Akt Pathway.

Yikui Tian, Bryan A Piras, Irving L Kron, Brent A French, Zequan Yang

Open access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.9field-weighted citation impact, top 10% 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

30 citing papers in PubMed, 57 citations in OpenAlex.

  1. Trial
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  6. Article
  7. Activation of AExperimental and therapeutic medicine · 2022
    Article
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  11. Review
  12. Article
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  15. Extracellular nucleotide signaling in solid organ transplantation.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2020
    Review
  16. Review
  17. Non-Nucleoside Agonists of the Adenosine Receptors: An Overview.Pharmaceuticals (Basel, Switzerland) · 2019
    Review
  18. Article
  19. Review
  20. Review
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

5 authors at 2 institutions in 2 countries.

Yikui TianDepartment of Surgery, University of Virginia, P.O. Box 800709, Charlottesville, VA 22908, USA ; Department of Cardiovascular Surgery, Tianjin Medical University General Hospital, Tianjin 300052, China.
Bryan A PirasDepartment of Biomedical Engineering, University of Virginia, Charlottesville, VA 22908, USA.
Irving L KronDepartment of Surgery, University of Virginia, P.O. Box 800709, Charlottesville, VA 22908, USA.
Brent A FrenchDepartment of Biomedical Engineering, University of Virginia, Charlottesville, VA 22908, USA.
Zequan YangDepartment of Surgery, University of Virginia, P.O. Box 800709, Charlottesville, VA 22908, USA ; Department of Biomedical Engineering, University of Virginia, Charlottesville, VA 22908, USA.
University of Virginia · USTianjin Medical University General Hospital · CN

Funding

Inflammation and Oxidative Stress in Hyperglycemic Exacerbation of Infarct SizeR01HL092305 · NHLBI · UNIVERSITY OF VIRGINIA · PI FRENCH, BRENT A, KRON, IRVING L. · 2009 to 2013
$1.9M
NHLBI NIH HHS R01 HL 092305NHLBI NIH HHS R01 HL092305
6 · The paper itself

Abstract

backgroundActivation of the adenosine A2B receptor (A2BR) can reduce myocardial ischemia/reperfusion (IR) injury. However, the mechanism underlying the A2BR-mediated cardioprotection is less clear. The present study was designed to investigate the potential mechanisms of cardioprotection mediated by A2BR. METHODS AND

resultsC57BL/6 mice underwent 40-minute ischemia and 60-minute reperfusion. ATL-801, a potent selective A2BR antagonist, could not block ischemic preconditioning induced protection. BAY 60-6583, a highly selective A2BR agonist, significantly reduced myocardial infarct size, and its protective effect could be blocked by either ATL-801 or wortmannin. BAY 60-6583 increased phosphorylated Akt (p-Akt) levels in the heart at 10 min of reperfusion, and this phosphorylation could also be blocked by ATL-801 or wortmannin. Furthermore, BAY 60-6583 significantly increased M2 macrophages and decreased M1 macrophage and neutrophils infiltration in reperfused hearts, which also could be blocked by wortmannin. Meanwhile, confocal imaging studies showed that the majority of Akt phosphorylation in the heart was colocalized to CD206+ cells in both control and BAY 60-6583 pretreated hearts.

conclusionOur results indicated that pretreatment with BAY 60-6583 protects the heart against myocardial IR injury by its anti-inflammatory effects, probably by modulating macrophages phenotype switching via a PI3K/Akt pathway.

Indexed as

Adenosine A2 Receptor AgonistsAdenosine A2 Receptor AntagonistsAminopyridinesAndrostadienesAnimalsCell DifferentiationHeart RateIschemic Preconditioning, MyocardialMacrophagesMaleMiceMice, Inbred C57BLMicroscopy, ConfocalMyocardial InfarctionMyocardial Reperfusion InjuryNeutrophil InfiltrationAdenosine A2 Receptor AgonistsAdenosine A2 Receptor AntagonistsAminopyridinesAndrostadienesBAY 60-6583Phosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReceptor, Adenosine A2BWortmannin

Identifiers

PMID26161239
PMCPMC4486757
OpenAlexW1551278092

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.