Evidence map›Paper›PMID 22652602›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2012

Selective β2-adrenoreceptor stimulation attenuates myocardial cell death and preserves cardiac function after ischemia-reperfusion injury.

Shashi Bhushan, Kazuhisa Kondo, Benjamin L Predmore, Maxim Zlatopolsky, Adrienne L King, Claire Pearce, Hui Huang, Ya-Xiong Tao, Marah E Condit, David J Lefer

Open access · greenAbstract read
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 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
2.0field-weighted citation impact, top 14% 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

21 citing papers in PubMed, 34 citations in OpenAlex.

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  11. Insulin and β Adrenergic Receptor Signaling: Crosstalk in Heart.Trends in endocrinology and metabolism: TEM · 2017
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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

10 authors at 1 institution in 1 country.

Shashi BhushanDepartment of Surgery, Division of Cardiothoracic Surgery, Emory University School of Medicine, 550 Peachtree St NE, Atlanta, GA 30308, USA.
Kazuhisa Kondo
Benjamin L Predmore
Maxim Zlatopolsky
Adrienne L King
Claire Pearce
Hui Huang
Ya-Xiong Tao
Marah E Condit
David J Lefer
Emory University Hospital Midtown · US

Funding

IRACDA Fellowships in Research and Science Training (FIRST)K12GM000680 · NIGMS · EMORY UNIVERSITY · PI BROWN, LOU ANN S, MCCARTY, NAEL A · 2000 to 2024
$41.2M
Preclinical Consortium to Facilitate Translation of Cardioprotective TherapiesU24HL094373 · NHLBI · UNIVERSITY OF LOUISVILLE · PI BOLLI, ROBERTO · 2010 to 2014
$9.6M
Cardioprotective Actions of Hydrogen SulfideR01HL092141 · NHLBI · LSU HEALTH SCIENCES CENTER · PI LEFER, DAVID JOSEPH · 2009 to 2013
$1.9M
Nitrite Mediated CardioprotectionR01HL093579 · NHLBI · LSU HEALTH SCIENCES CENTER · PI LEFER, DAVID JOSEPH · 2009 to 2012
$1.5M
NHLBI NIH HHS 5R01HL092141-03NHLBI NIH HHS 5R01HL093579-03NHLBI NIH HHS 5U24HL094373-02NHLBI NIH HHS R01 HL092141NHLBI NIH HHS R01 HL093579NHLBI NIH HHS U24 HL094373NIGMS NIH HHS K12 GM000680
6 · The paper itself

Abstract

objectiveβ(2)-adrenoreceptor activation has been shown to protect cardiac myocytes from cell death. We hypothesized that acute β(2)-adrenoreceptor stimulation, using arformoterol (ARF), would attenuate myocardial ischemia/reperfusion (R) injury via NO synthase activation and cause a subsequent increase in NO bioavailability. METHODS AND

resultsMale C57BL/6J and endothelial NO synthase (eNOS) knockout mice were subjected to 45 minutes of myocardial ischemia and 24 hours of R. ARF or vehicle was administered 5 minutes before R. Serum troponin-I was measured, and infarct size per area-at-risk was evaluated at 24 hours of R. Echocardiography was performed at baseline and 2 weeks after R. Myocardial cAMP, protein kinase A, eNOS/Akt phosphorylation status, and NO metabolite levels were assayed. ARF (1 µg/kg) reduced infarct size per area-at-risk by 53.1% (P<0.001 versus vehicle) and significantly reduced troponin-I levels (P<0.001 versus vehicle). Ejection fraction was significantly preserved in ARF-treated hearts compared with vehicle hearts at 2 weeks of R. Serum cAMP and nuclear protein kinase A C-α increased 5 and 15 minutes after ARF injection, respectively (P<0.01). ARF increased Akt phosphorylation at Thr(308) (P<0.001) and Ser(473) (P<0.01), and eNOS phosphorylation at Ser(1177) (P<0.01). ARF treatment increased heart nitrosothiol levels (P<0.001) at 15 min after injection. ARF failed to reduce infarct size in eNOS(-/-) mice.

conclusionsOur results indicate that β(2)-adrenoreceptor stimulation activates cAMP, protein kinase A, Akt, and eNOS and augments NO bioavailability. Activation of this prosurvival signaling pathway attenuates myocardial cell death and preserves cardiac function after ischemia/reperfusion.

Indexed as

Adrenergic beta-2 Receptor AgonistsAnimalsCell DeathCyclic AMP-Dependent Protein KinasesEthanolaminesFormoterol FumarateIschemic Preconditioning, MyocardialMaleMiceMice, Inbred C57BLMyocardial Reperfusion InjuryMyocytes, CardiacNitric Oxide Synthase Type IIIProto-Oncogene Proteins c-aktAdrenergic beta-2 Receptor AgonistsCyclic AMP-Dependent Protein KinasesEthanolaminesFormoterol FumarateNitric Oxide Synthase Type IIINos3 protein, mouseProto-Oncogene Proteins c-akt

Identifiers

PMID22652602
PMCPMC3401356
OpenAlexW2128259987

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.