Evidence map›Paper›PMID 35567658›Full record

ReviewCurrent heart failure reports2022

Targeting Myocardial Substrate Metabolism in the Failing Heart: Ready for Prime Time?

Salva R Yurista, Shi Chen, Aidan Welsh, W H Wilson Tang, Christopher T Nguyen

Open access · greenAbstract readReview
In one paragraph

Review in Current heart failure reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
3.4field-weighted citation impact, top 6% 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

17 citing papers in PubMed, 21 citations in OpenAlex.

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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 1 country.

Salva R YuristaCardiovascular Research Center, Corrigan Minehan Heart Center, Massachusetts General Hospital, Harvard Medical School, 149 13th Street, Boston, MA, 02129, USA. syurista@mgh.harvard.edu.
Shi ChenCardiovascular Research Center, Corrigan Minehan Heart Center, Massachusetts General Hospital, Harvard Medical School, 149 13th Street, Boston, MA, 02129, USA.
Aidan WelshCardiovascular Research Center, Corrigan Minehan Heart Center, Massachusetts General Hospital, Harvard Medical School, 149 13th Street, Boston, MA, 02129, USA.
W H Wilson TangHeart, Vascular, and Thoracic Institute, Cleveland Clinic, Cleveland, OH, USA.
Christopher T NguyenCardiovascular Research Center, Corrigan Minehan Heart Center, Massachusetts General Hospital, Harvard Medical School, 149 13th Street, Boston, MA, 02129, USA.
Massachusetts General Hospital · USAthinoula A. Martinos Center for Biomedical Imaging · USCleveland Clinic · USHarvard University · US

Funding

Serial evaluation of cardioprotective effects of exercise training in heart failure using cardiac diffusion tensor MRIR01HL151704 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI NGUYEN, CHRISTOPHER T · 2020 to 2024
$3.4M
Microstructural Response of the Myocardium to Mechanical LoadR01HL159010 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI MEKKAOUI, CHOUKRI, NGUYEN, CHRISTOPHER T · 2021 to 2024
$3.2M
Stress-rest calf muscle perfusion: a functional diagnostic test for peripheral arterial disease (PAD)R01HL135242 · NHLBI · UNIVERSITY OF UTAH · PI NATARAJAN, PRADEEP · 2017 to 2020
$2.8M
Modeling, measurement and prediction of cardiac magneto-stimulation thresholdsR01EB033853 · NIBIB · MASSACHUSETTS GENERAL HOSPITAL · PI Bastien Guerin, Christopher T Nguyen · 2023 to 2026
$2.4M
NHLBI NIH HHS R01 HL135242NHLBI NIH HHS R01 HL151704NHLBI NIH HHS R01 HL159010NIBIB NIH HHS R01 EB033853NIH HHS R01 HL135242NIH HHS R01 HL151704NIH HHS R01 HL159010
6 · The paper itself

Abstract

purpose of reviewWe review the clinical benefits of altering myocardial substrate metabolism in heart failure. RECENT

findingsModulation of cardiac substrates (fatty acid, glucose, or ketone metabolism) offers a wide range of therapeutic possibilities which may be applicable to heart failure. Augmenting ketone oxidation seems to offer great promise as a new therapeutic modality in heart failure. The heart has long been recognized as metabolic omnivore, meaning it can utilize a variety of energy substrates to maintain adequate ATP production. The adult heart uses fatty acid as a major fuel source, but it can also derive energy from other substrates including glucose and ketone, and to some extent pyruvate, lactate, and amino acids. However, cardiomyocytes of the failing heart endure remarkable metabolic remodeling including a shift in substrate utilization and reduced ATP production, which account for cardiac remodeling and dysfunction. Research to understand the implication of myocardial metabolic perturbation in heart failure has grown in recent years, and this has raised interest in targeting myocardial substrate metabolism for heart failure therapy. Due to the interdependency between different pathways, the main therapeutic metabolic approaches include inhibiting fatty acid uptake/fatty acid oxidation, reducing circulating fatty acid levels, increasing glucose oxidation, and augmenting ketone oxidation.

Indexed as

Heart FailureAdenosine TriphosphateAdultEnergy MetabolismFatty AcidsGlucoseHumansKetonesMyocardiumAdenosine TriphosphateFatty AcidsGlucoseKetonesCardiac metabolismFatty acidGlucoseHeart failureKetone bodies

Identifiers

PMID35567658
PMCPMC10950325
OpenAlexW4280530579

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.