Evidence map›Paper›PMID 19695259›Full record

ArticleJournal of molecular and cellular cardiology2009

Adenosine A2A and A2B receptors work in concert to induce a strong protection against reperfusion injury in rat hearts.

Jinkun Xi, Rachel McIntosh, Xiangjun Shen, SungRyul Lee, Guillaume Chanoit, Hugh Criswell, David A Zvara, Zhelong Xu

Abstract read
In one paragraph

Article in Journal of molecular and cellular cardiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
7.1field-weighted citation impact, top 3% 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

46 citing papers in PubMed, 83 citations in OpenAlex.

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  11. Ranolazine may exert its beneficial effects by increasing myocardial adenosine levels.American journal of physiology. Heart and circulatory physiology · 2020
    Article
  12. Role of Cardiac AFrontiers in pharmacology · 2020
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  15. Therapeutic Ultrasound Increases Myocardial Blood Flow in Ischemic Myocardium and Cardiac Endothelial Cells: Results of In Vivo and In Vitro Experiments.Journal of the American Society of Echocardiography : official publication of the American Society of Echocardiography · 2019
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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

8 authors at 1 institution in 1 country.

Jinkun XiDepartment of Anesthesiology, The University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.
Rachel McIntosh
Xiangjun Shen
SungRyul Lee
Guillaume Chanoit
Hugh Criswell
David A Zvara
Zhelong Xu
University of North Carolina at Chapel Hill · US

Funding

Effect of Adenosine A2 receptor activation on the mitochondrial death pathwayR01HL083362 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI XU, ZHELONG · 2006 to 2010
$2.0M
NHLBI NIH HHS R01-HL-08336NHLBI NIH HHS R01 HL083362
6 · The paper itself

Abstract

We aimed to test if stimulation of both adenosine A2A and A2B receptors is required to produce an effective cardioprotection against reperfusion injury. Isolated rat hearts were subjected to 30-min regional ischemia followed by 2 h of reperfusion. The adenosine A1/A2 receptor agonist 5'-(N-ethylcarboxamido) adenosine (NECA) given at reperfusion reduced infarct size, an effect that was reversed by both the adenosine A2A antagonist SCH58261 and the A2B antagonist MRS1706. The A2B agonist BAY 60-6583 but not the selective A2A agonist CGS21680 reduced infarct size. Interestingly, a combination of BAY 60-6583 and CGS21680 further reduced infarct size. These results suggest that both A2A and A2B receptors are involved in NECA's anti-infarct effect at reperfusion. NECA attenuated mitochondrial swelling upon reperfusion and this was blocked by both SCH58261 and MRS1706, indicating that activation of A2 receptors with NECA can modulate reperfusion-induced mitochondrial permeability transition pore (mPTP) opening. In support, NECA also prevented oxidant-induced loss of mitochondrial membrane potential (DeltaPsi(m)) and matrix Ca2+ overload in cardiomyocytes via both the A2 receptors. In addition, NECA increased mitochondrial glycogen synthase kinase-3beta (GSK-3beta) phosphorylation upon reperfusion and this was again blocked by SCH58261 and MRS1706. In conclusion, A2A and A2B receptors work in concert to prevent reperfusion injury in rat hearts treated with NECA. NECA may protect the heart by modulating the mPTP opening through inactivating mitochondrial GSK-3beta. A simultaneous stimulation of A2A and A2B receptors at reperfusion is required to produce a strong cardioprotection against reperfusion injury.

Indexed as

Adenosine-5'-(N-ethylcarboxamide)AnimalsBlotting, WesternHeartMaleMicroscopy, ConfocalMyocardiumMyocytes, CardiacRatsRats, WistarReceptor, Adenosine A2AReceptor, Adenosine A2BReperfusion InjuryReverse Transcriptase Polymerase Chain ReactionVasodilator AgentsAdenosine-5'-(N-ethylcarboxamide)Receptor, Adenosine A2AReceptor, Adenosine A2BVasodilator Agents

Identifiers

PMID19695259
PMCPMC2782744
OpenAlexW1985927695

What OpenQuestion holds

Textmetadata
LicenceTDM
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.