Evidence map›Paper›PMID 19552606›Full record

ArticleAntioxidants & redox signaling2009

Endogenous adenosine selectively modulates oxidant stress via the A1 receptor in ischemic hearts.

Melissa E Reichelt, Anu Shanu, Laura Willems, Paul K Witting, Natasha A Ellis, Michael R Blackburn, John P Headrick

Open access · greenAbstract read
In one paragraph

Article in Antioxidants & redox signaling, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
0.6field-weighted citation impact, top 28% 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

14 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.

  1. Pooled it
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  14. Adenosine kinase regulation of cardiomyocyte hypertrophy.American journal of physiology. Heart and circulatory physiology · 2011
    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

7 authors at 4 institutions in 2 countries.

Melissa E ReicheltHeart Foundation Research Center, Griffith University , Southport, Queensland, Australia. mreichelt@ucsd.edu
Anu Shanu
Laura Willems
Paul K Witting
Natasha A Ellis
Michael R Blackburn
John P Headrick
Griffith University · AUThe University of Sydney · AUConcord Repatriation General Hospital · AUThe University of Texas Health Science Center at Houston · US

Funding

Molecular Models of Adenosine Signaling and AsthmaR01AI043572 · NIAID · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI BLACKBURN, MICHAEL R · 1998 to 2008
$1.8M
NIAID NIH HHS AI-43572
6 · The paper itself

Abstract

We tested the impact of A1 adenosine receptor (AR) deletion on injury and oxidant damage in mouse hearts subjected to 25-min ischemia/45-min reperfusion (I/R). Wild-type hearts recovered approximately 50% of contractile function and released 8.2 +/- 0.7 IU/g of lactate dehydrogenase (LDH). A1AR deletion worsened dysfunction and LDH efflux (15.2 +/- 2.6 IU/g). Tissue cholesterol and native cholesteryl esters were unchanged, whereas cholesteryl ester-derived lipid hydroperoxides and hydroxides (CE-O(O)H; a marker of lipid oxidation) increased threefold, and alpha-tocopherylquinone [alpha-TQ; oxidation product of alpha-tocopherol (alpha-TOH)] increased sixfold. Elevations in alpha-TQ were augmented by two- to threefold by A1AR deletion, whereas CE-O(O)H was unaltered. A(1)AR deletion also decreased glutathione redox status ([GSH]/[GSSG + GSH]) and enhanced expression of the antioxidant response element heme oxygenase-1 (HO-1) during I/R: fourfold elevations in HO-1 mRNA and activity were doubled by A1AR deletion. Broad-spectrum AR agonism (10 microM 2-chloroadenosine; 2-CAD) countered effects of A1AR deletion on oxidant damage, HO-1, and tissue injury, indicating that additional ARs (A(2A), A(2B), and/or A3) can mediate similar actions. These data reveal that local adenosine engages A1ARs during I/R to limit oxidant damage and enhance outcome selectively. Control of alpha-TOH/alpha-TQ levels may contribute to A1AR-dependent cardioprotection.

Indexed as

2-ChloroadenosineAdenosineAdenosine A1 Receptor AgonistsAnimalsCholesterolCholesterol EstersChromatography, High Pressure LiquidGlutathioneHeme Oxygenase-1HydroxidesLipid PeroxidesL-Lactate DehydrogenaseMaleMiceMyocardial Reperfusion InjuryOxidation-Reduction2-ChloroadenosineAdenosineAdenosine A1 Receptor AgonistsCholesterolCholesterol EstersGlutathioneHeme Oxygenase-1HydroxidesLipid PeroxidesL-Lactate DehydrogenaseReceptor, Adenosine A1tocopherylquinoneVitamin E

Identifiers

PMID19552606
PMCPMC2861535
OpenAlexW2006023285

What OpenQuestion holds

Textmetadata
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.