Evidence map›Paper›PMID 17573462›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2007

Increased O-GlcNAc levels during reperfusion lead to improved functional recovery and reduced calpain proteolysis.

Jia Liu, Richard B Marchase, John C Chatham

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed
4.2field-weighted citation impact, top 5% 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

69 citing papers in PubMed, 114 citations in OpenAlex.

  1. Trial
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  7. Review
  8. Review
  9. O-GlcNAcylation in ischemic diseases.Frontiers in pharmacology · 2024
    Review
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  11. Review
  12. Review
  13. Article
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9 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Jia LiuDepartment of Cell Biology, University of Alabama at Birmingham, AL 35294-0005, USA.
Richard B Marchase
John C Chatham
University of Alabama at Birmingham · US

Funding

The Impact on Diabetes on Left Ventricular RemodelingP50HL077100 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI DELL'LTALIA, LOUIS · 2005 to 2009
$16.5M
TYPE 2 DIABETES AND CARDIAC DYSFUNCTIONR01HL067464 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI CHATHAM, JOHN C · 2000 to 2009
$1.9M
Mechanisms of glucosamine ischemic cardioprotectionR01HL079364 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI CHATHAM, JOHN C · 2006 to 2010
$1.9M
Cytoplasmic Glycosylation and Hypovolemic StressR01HL076175 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI MARCHASE, RICHARD BANFIELD · 2004 to 2007
$1.4M
NHLBI NIH HHS HL-076175NHLBI NIH HHS HL-077100NHLBI NIH HHS HL-079364NHLBI NIH HHS HL-67464NHLBI NIH HHS P50 HL077100NHLBI NIH HHS R01 HL067464NHLBI NIH HHS R01 HL076175NHLBI NIH HHS R01 HL079364
6 · The paper itself

Abstract

We have previously shown that preischemic treatment with glucosamine improved cardiac functional recovery following ischemia-reperfusion, and this was mediated, at least in part, via enhanced flux through the hexosamine biosynthesis pathway and subsequently elevated O-linked N-acetylglucosamine (O-GlcNAc) protein levels. However, preischemic treatment is typically impractical in a clinical setting; therefore, the goal of this study was to investigate whether increasing protein O-GlcNAc levels only during reperfusion also improved recovery. Isolated perfused rat hearts were subjected to 20 min of global, no-flow ischemia followed by 60 min of reperfusion. Administration of glucosamine (10 mM) or an inhibitor of O-GlcNAcase, O-(2-acetamido-2-deoxy-D-glucopyranosylidene)amino-N-phenylcarbamate (PUGNAc; 200 microM), during the first 20 min of reperfusion significantly improved cardiac functional recovery and reduced troponin release during reperfusion compared with untreated control. Both interventions also significantly increased the levels of protein O-GlcNAc and ATP levels. We also found that both glucosamine and PUGNAc attenuated calpain-mediated proteolysis of alpha-fodrin as well as Ca(2+)/calmodulin-dependent protein kinase II during reperfusion. Thus two independent strategies for increasing protein O-GlcNAc levels in the heart during reperfusion significantly improved recovery, and this was correlated with attenuation of calcium-mediated proteolysis. These data provide further support for the concept that increasing cardiac O-GlcNAc levels may be a clinically relevant cardioprotective strategy and suggest that this protection could be due, at least in part, to inhibition of calcium-mediated stress responses.

Indexed as

AcetylglucosamineAdenosine TriphosphateAnimalsCalciumCalcium-Calmodulin-Dependent Protein KinasesCalcium-Calmodulin-Dependent Protein Kinase Type 2CalpainCarrier ProteinsGlucosamineMicrofilament ProteinsMyocardial IschemiaMyocardial Reperfusion InjuryMyocardiumOximesPhenylcarbamatesRatsAcetylglucosamineAdenosine TriphosphateCalciumCalcium-Calmodulin-Dependent Protein KinasesCalcium-Calmodulin-Dependent Protein Kinase Type 2CalpainCarrier ProteinsGlucosamineMicrofilament ProteinsN-acetylglucosaminono-1,5-lactone O-(phenylcarbamoyl)oximeOximesPhenylcarbamatesSpectrin

Identifiers

PMID17573462
PMCPMC2850209
OpenAlexW2149696055

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.