Evidence map›Paper›PMID 28944310›Full record

ArticleJACC. Basic to translational science2017

Metabolic Origins of Heart Failure.

Adam R Wende, Manoja K Brahma, Graham R McGinnis, Martin E Young

Abstract read
In one paragraph

Article in JACC. Basic to translational science, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 127 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
127citing papers in PubMed, 3 pooled it
–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

127 citing papers in PubMed, 3 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Trial
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  7. Article
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  10. Review
  11. Article
  12. Article
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  14. Cellular and molecular signals of cardiac wound healing after myocardial infarction.American journal of physiology. Heart and circulatory physiology · 2026
    Review
  15. Observational
  16. Review
  17. Article
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  20. Observational

67 more citing papers are in PubMed but not listed here.

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

4 authors.

Adam R WendeDepartment of Pathology, University of Alabama at Birmingham, Birmingham, AL, USA.
Manoja K BrahmaDepartment of Pathology, University of Alabama at Birmingham, Birmingham, AL, USA.
Graham R McGinnisDepartment of Medicine, University of Alabama at Birmingham, Birmingham, AL, USA.
Martin E YoungDepartment of Medicine, University of Alabama at Birmingham, Birmingham, AL, USA.

Funding

Why is the prevalence of obesity so high in U.S. Southern States? Regional predictors of BMI and obesity treatment response.P30DK056336 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BARBARA A GOWER · 2000 to 2026
$31.9M
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
Disruption of the Clock O-GlcNAc axis in diabetic cardiomyopathyR01HL122975 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI CHATHAM, JOHN C, YOUNG, MARTIN E · 2015 to 2018
$1.6M
Circadian Regulation of Myocardial Insulin SignalingR01HL123574 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI YOUNG, MARTIN E · 2014 to 2017
$1.5M
Glucose-Mediated Remodeling of Cardiac DNA MethylationR01HL133011 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI WENDE, ADAM RAYMOND · 2017 to 2020
$1.5M
Mechanisms of glucose mediated cardiac mitochondrial dysfunctionR00HL111322 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI WENDE, ADAM RAYMOND · 2013 to 2015
$870k
Time-of-Day-Dependent Feeding Influences Myocardial FunctionR21HL106199 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI YOUNG, MARTIN E · 2011 to 2012
$403k
Glucose-Mediated Remodeling of Cardiac DNA MethylationR56HL133011 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI WENDE, ADAM RAYMOND · 2016 to 2016
$368k
Mechanisms of glucose mediated cardiac mitochondrial dysfunctionK99HL111322 · NHLBI · UNIVERSITY OF UTAH · PI WENDE, ADAM RAYMOND · 2012 to 2013
$274k
NHLBI NIH HHS K99 HL111322NHLBI NIH HHS R00 HL111322NHLBI NIH HHS R01 HL074259NHLBI NIH HHS R01 HL122975NHLBI NIH HHS R01 HL123574NHLBI NIH HHS R01 HL133011NHLBI NIH HHS R21 HL106199NHLBI NIH HHS R56 HL133011NIDDK NIH HHS P30 DK056336NIDDK NIH HHS P30 DK079626
6 · The paper itself

Abstract

For more than half a century, metabolic perturbations have been explored in the failing myocardium, highlighting a reversion to a more fetal-like metabolic profile (characterized by depressed fatty acid oxidation and concomitant increased reliance on glucose utilization). More recently, alterations in ketone body and amino acid/protein metabolism have been described during heart failure, as well as mitochondrial dysfunction and perturbed metabolic signaling (e.g., acetylation, O-GlcNAcylation). Although numerous mechanisms are likely involved, the current review provides recent advances regarding the metabolic origins of heart failure, and their potential contribution toward contractile dysfunction of the heart.

Indexed as

amino acidsfatty acidsglucoseheart failureketone bodies

Identifiers

PMID28944310
PMCPMC5609457

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.