Evidence map›Paper›PMID 22766272›Full record

ReviewJournal of molecular and cellular cardiology2013

Regulation of myocardial metabolism by the cardiomyocyte circadian clock.

John C Chatham, Martin E Young

Abstract readReview
In one paragraph

Review in Journal of molecular and cellular cardiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
–field-weighted citation impact
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

23 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. The Circadian Biology of Heart Failure.Circulation research · 2023
    Review
  5. Article
  6. Review
  7. Review
  8. Review
  9. A metabocentric view of cardiac remodeling.Current opinion in physiology · 2019
    Article
  10. Old and New Roles and Evolving Complexities of Cardiovascular Clocks.The Yale journal of biology and medicine · 2019
    Review
  11. Review
  12. Circadian Rhythm, Lifestyle and Health: A Narrative Review.Iranian journal of public health · 2018
    Review
  13. Review
  14. Review
  15. Metabolic Mechanisms of Exercise-Induced Cardiac Remodeling.Frontiers in cardiovascular medicine · 2018
    Review
  16. Review
  17. Article
  18. Article
  19. Review
  20. 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

2 authors.

John C ChathamDivision of Molecular and Cellular Pathology, Department of Pathology, University of Alabama at Birmingham, Birmingham, AL 35294, USA.
Martin E Young

Funding

University of Alabama at Birmingham's Diabetes Research CenterP30DK079626 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI Kirk Michael Habegger · 2013 to 2026
$19.5M
Role of the Molecular Circadian Clock within the HeartR01HL074259 · NHLBI · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI YOUNG, MARTIN E · 2004 to 2012
$3.1M
Mechanisms of glucosamine ischemic cardioprotectionR01HL079364 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI CHATHAM, JOHN C · 2006 to 2010
$1.9M
Protein O-GlcNAcylation and the regulation of cardiac functionR01HL101192 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI CHATHAM, JOHN C · 2010 to 2014
$1.5M
Time-of-Day-Dependent Feeding Influences Myocardial FunctionR21HL106199 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI YOUNG, MARTIN E · 2011 to 2012
$403k
Influence of the Cardiomyocyte Circadian Clock on Cardiac HypertrophyR21HL107709 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI YOUNG, MARTIN E · 2012 to 2013
$392k
NHLBI NIH HHS HL-074259NHLBI NIH HHS HL079364NHLBI NIH HHS HL101192NHLBI NIH HHS HL-106199NHLBI NIH HHS R01 HL074259NHLBI NIH HHS R01 HL079364NHLBI NIH HHS R01 HL101192NHLBI NIH HHS R21 HL106199NHLBI NIH HHS R21 HL107709NIDDK NIH HHS P30 DK079626
6 · The paper itself

Abstract

On a daily basis, the heart is subjected to dramatic fluctuations in energetic demand and neurohumoral influences, many of which occur in a temporally predictable manner. In order to preserve cardiac performance, the heart must therefore maintain metabolic flexibility, even within the confines of a single day. Recent studies have established mechanistic links between time-of-day-dependent oscillations in myocardial metabolism and the cardiomyocyte circadian clock. More specifically, evidence suggests that this cell autonomous molecular mechanism regulates myocardial glucose uptake, flux through both glycolysis and the hexosamine biosynthetic pathway, and pyruvate oxidation, as well as glycogen, triglyceride, and protein turnover. These observations have led to the hypothesis that the cardiomyocyte circadian clock confers the selective advantage of anticipation of increased energetic demand during the awake period. Here, we review the accumulative evidence in support of this hypothesis thus far, and discuss the possibility that attenuation of these metabolic rhythms, through disruption of the cardiomyocyte circadian clock, contributes towards the etiology of cardiac dysfunction in various disease states. This article is part of a Special Issue entitled "Focus on Cardiac Metabolism".

Indexed as

AnimalsCircadian ClocksCircadian RhythmEnergy MetabolismHumansMyocardiumMyocytes, Cardiac

Identifiers

PMID22766272
PMCPMC4107417

What OpenQuestion holds

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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.