Evidence map›Paper›PMID 33983836›Full record

ReviewCirculation research2021

Cardiac Energy Metabolism in Heart Failure.

Gary D Lopaschuk, Qutuba G Karwi, Rong Tian, Adam R Wende, E Dale Abel

Open access · bronzeAbstract readReview
In one paragraph

Review in Circulation research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 854 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
854citing papers in PubMed, 2 pooled it
115.2field-weighted citation impact, top 1% 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

854 citing papers in PubMed, 2 syntheses or guidelines pooled it, 1,195 citations in OpenAlex.

  1. Pooled it
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  6. Article
  7. Article
  8. Review
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  13. Energy constraint on human health.Trends in endocrinology and metabolism: TEM · 2026
    Review
  14. Article
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  16. Review
  17. Review
  18. Review
  19. Timed metabolic repair after myocardial infarction.Nature cardiovascular research · 2026
    Article
  20. Article

794 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

5 authors at 4 institutions in 2 countries.

Gary D LopaschukCardiovascular Research Centre, University of Alberta, Edmonton, Canada (G.D.L., Q.G.K.).
Qutuba G KarwiCardiovascular Research Centre, University of Alberta, Edmonton, Canada (G.D.L., Q.G.K.).
Rong TianMitochondria and Metabolism Center, University of Washington, Seattle (R.T.).
Adam R WendeDivision of Molecular and Cellular Pathology, Department of Pathology, University of Alabama at Birmingham (A.R.W.).
E Dale AbelDivision of Endocrinology and Metabolism, University of Iowa Carver College of Medicine, Iowa City (E.D.A.).
University of Alberta · CAMitochondria Research and Medicine Society · USUniversity of Alabama at Birmingham · USUniversity of Iowa · US

Funding

NAD+/NADH ratio, protein acetylation and mitochondrial functionR01HL110349 · NHLBI · UNIVERSITY OF WASHINGTON · PI TIAN, RONG · 2011 to 2020
$5.7M
Mechanistic Studies of NAD+/NADH in Human Heart FailureR01HL144937 · NHLBI · UNIVERSITY OF WASHINGTON · PI O'BRIEN, KEVIN D., TIAN, RONG · 2019 to 2023
$4.2M
Fatty acid oxidation suppresses cardiac hypertrophyR01HL129510 · NHLBI · UNIVERSITY OF WASHINGTON · PI TIAN, RONG · 2015 to 2018
$2.8M
Insulin Inhibition of beta-AR Signaling in the MyocardiumR01HL127764 · NHLBI · UNIVERSITY OF IOWA · PI ABEL, E DALE, XIANG, YANG K · 2015 to 2018
$2.4M
Mitochondrial function and glycolytic switch in pathological cardiac hypertrophyR01HL142628 · NHLBI · UNIVERSITY OF WASHINGTON · PI TIAN, RONG · 2018 to 2021
$2.4M
OPA1 an Estrogen-Mediated Modulator of Platelet HyperactivationR33HL141783 · NHLBI · UNIVERSITY OF IOWA · PI ABEL, E DALE, RONDINA, MATTHEW THOMAS · 2020 to 2022
$2.2M
Cardiac Dysfunction in the Met Syndrome: Cross-talk between IR and bAR SignalingR01HL112413 · NHLBI · UNIVERSITY OF IOWA · PI ABEL, E DALE, XIANG, YANG K · 2015 to 2018
$1.6M
Glucose-Mediated Remodeling of Cardiac DNA MethylationR01HL133011 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI WENDE, ADAM RAYMOND · 2017 to 2020
$1.5M
OPA1 an Estrogen-Mediated Modulator of Platelet HyperactivationR61HL141783 · NHLBI · UNIVERSITY OF IOWA · PI ABEL, E DALE, WEYRICH, ANDREW S · 2018 to 2019
$1.5M
The role of protein O-linked N-Acetylglucosamine in regulating cardiac physiologyR21HL152354 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI CHATHAM, JOHN C, WENDE, ADAM RAYMOND · 2020 to 2021
$408k
Glucose-Mediated Remodeling of Cardiac DNA MethylationR56HL133011 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI WENDE, ADAM RAYMOND · 2016 to 2016
$368k
Canadian Institute for Health ResearchNHLBI NIH HHS R01 HL110349NHLBI NIH HHS R01 HL112413NHLBI NIH HHS R01 HL127764NHLBI NIH HHS R01 HL129510NHLBI NIH HHS R01 HL133011NHLBI NIH HHS R01 HL142628NHLBI NIH HHS R01 HL144937NHLBI NIH HHS R21 HL152354NHLBI NIH HHS R33 HL141783NHLBI NIH HHS R56 HL133011NHLBI NIH HHS R61 HL141783
6 · The paper itself

Abstract

Alterations in cardiac energy metabolism contribute to the severity of heart failure. However, the energy metabolic changes that occur in heart failure are complex and are dependent not only on the severity and type of heart failure present but also on the co-existence of common comorbidities such as obesity and type 2 diabetes. The failing heart faces an energy deficit, primarily because of a decrease in mitochondrial oxidative capacity. This is partly compensated for by an increase in ATP production from glycolysis. The relative contribution of the different fuels for mitochondrial ATP production also changes, including a decrease in glucose and amino acid oxidation, and an increase in ketone oxidation. The oxidation of fatty acids by the heart increases or decreases, depending on the type of heart failure. For instance, in heart failure associated with diabetes and obesity, myocardial fatty acid oxidation increases, while in heart failure associated with hypertension or ischemia, myocardial fatty acid oxidation decreases. Combined, these energy metabolic changes result in the failing heart becoming less efficient (ie, a decrease in cardiac work/O

Indexed as

Energy MetabolismAdenosine TriphosphateAmino Acids, Branched-ChainComorbidityDiabetes Mellitus, Type 2Epigenesis, GeneticFatty AcidsGlucoseGlycolysisHeart FailureHumansInsulin ResistanceKetone BodiesMitochondriaMyocardiumNADAdenosine TriphosphateAmino Acids, Branched-ChainFatty AcidsGlucoseKetone BodiesNADacetylationdiabetic cardiomyopathiesinsulin resistanceketonesmitochondria

Identifiers

PMID33983836
PMCPMC8136750
OpenAlexW3160863677

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.