Evidence map›Paper›PMID 29929976›Full record

ReviewCirculation research2018

Metabolic Coordination of Physiological and Pathological Cardiac Remodeling.

Andrew A Gibb, Bradford G Hill

Abstract readReview
In one paragraph

Review in Circulation research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 249 papers.

0numbers the graph read from it
0cells of the map it votes in
249citing 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

249 citing papers in PubMed.

  1. Intravenous regular insulin is an efficient and safe procedure for obtaining high-quality cardiacJournal of nuclear cardiology : official publication of the American Society of Nuclear Cardiology · 2022
    Trial
  2. Review
  3. An integrated overview of acute heart failure: a narrative review of pathophysiological mechanisms and contributing factors.The Egyptian heart journal : (EHJ) : official bulletin of the Egyptian Society of Cardiology · 2026
    Review
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189 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

2 authors.

Andrew A GibbFrom the Center for Translational Medicine, Lewis Katz School of Medicine, Temple University, Philadelphia, PA (A.A.G.).
Bradford G Hillthe Department of Medicine, Institute of Molecular Cardiology, Diabetes and Obesity Center, University of Louisville School of Medicine, KY (B.G.H.). bradford.hill@louisville.edu.

Funding

Tumor Necrosis Factor Modulation of CPCsP01HL078825 · NHLBI · UNIVERSITY OF LOUISVILLE · PI BOLLI, ROBERTO · 2005 to 2021
$37.6M
Metabolic optimization of cell therapyR01HL130174 · NHLBI · UNIVERSITY OF LOUISVILLE · PI HILL, BRADFORD GUY · 2016 to 2020
$1.9M
Metabolic regulation of cardiac stem cellsR56HL122580 · NHLBI · UNIVERSITY OF LOUISVILLE · PI HILL, BRADFORD GUY · 2015 to 2015
$381k
American Heart Association-American Stroke Association 16PRE31010022NHLBI NIH HHS P01 HL078825NHLBI NIH HHS R01 HL130174NHLBI NIH HHS R56 HL122580
6 · The paper itself

Abstract

Metabolic pathways integrate to support tissue homeostasis and to prompt changes in cell phenotype. In particular, the heart consumes relatively large amounts of substrate not only to regenerate ATP for contraction but also to sustain biosynthetic reactions for replacement of cellular building blocks. Metabolic pathways also control intracellular redox state, and metabolic intermediates and end products provide signals that prompt changes in enzymatic activity and gene expression. Mounting evidence suggests that the changes in cardiac metabolism that occur during development, exercise, and pregnancy as well as with pathological stress (eg, myocardial infarction, pressure overload) are causative in cardiac remodeling. Metabolism-mediated changes in gene expression, metabolite signaling, and the channeling of glucose-derived carbon toward anabolic pathways seem critical for physiological growth of the heart, and metabolic inefficiency and loss of coordinated anabolic activity are emerging as proximal causes of pathological remodeling. This review integrates knowledge of different forms of cardiac remodeling to develop general models of how relationships between catabolic and anabolic glucose metabolism may fortify cardiac health or promote (mal)adaptive myocardial remodeling. Adoption of conceptual frameworks based in relational biology may enable further understanding of how metabolism regulates cardiac structure and function.

Indexed as

Adaptation, PhysiologicalAdenosine TriphosphateCardiomegalyCardiomegaly, Exercise-InducedDiabetes MellitusEnergy MetabolismExerciseFemaleFetal HeartGene ExpressionGlucoseHeartHeart FailureHumansMyocardiumPregnancyAdenosine TriphosphateGlucoseexerciseglucoseheart failurehypertrophymitochondriapregnancysystems biology

Identifiers

PMID29929976
PMCPMC6023588

What OpenQuestion holds

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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.