Evidence map›Paper›PMID 22728216›Full record

ReviewJournal of molecular and cellular cardiology2013

Metabolic stress in the myocardium: adaptations of gene expression.

Peter A Crawford, Jean E Schaffer

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 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing 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

9 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. A model of chronic nutrient infusion in the rat.Journal of visualized experiments : JoVE · 2013
    Article
  9. 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.

Peter A CrawfordDiabetic Cardiovascular Disease Center, Cardiovascular Division, Washington University School of Medicine, USA. pcrawford@wustl.edu
Jean E Schaffer

Funding

KETONE BODY METABOLISM AND INTEGRATED METABOLIC HOMEOSTASISR01DK091538 · NIDDK · WASHINGTON UNIVERSITY · PI CRAWFORD, PETER A · 2011 to 2024
$6.2M
CELLULAR MECHANISMS THAT PROMOTE OR PREVENT LIPOTOXICITYR01DK064989 · NIDDK · WASHINGTON UNIVERSITY · PI SCHAFFER, JEAN E. · 2003 to 2021
$5.8M
Lipid Biomarkers for Diabetic Heart DiseaseP20HL113444 · NHLBI · WASHINGTON UNIVERSITY · PI SCHAFFER, JEAN E. · 2012 to 2016
$4.7M
NHLBI NIH HHS P20 HL113444NIDDK NIH HHS R01 DK064989NIDDK NIH HHS R01 DK091538
6 · The paper itself

Abstract

The heart is one of the highest ATP consuming organs in mammalian organisms. Its metabolic function has evolved a remarkable degree of efficiency to meet high demand and plasticity in response to varying changes in energy substrate supply. Given the high flux of energy substrates and the centrality of their appropriate use for optimal cardiac function, it is not surprising that the heart has intricate signaling mechanisms through which it responds to metabolic stress. This review focuses on the changes in gene expression in myocardial and vascular tissues during metabolic stress that affect mRNAs and subsequent protein synthesis with an eye toward understanding the manner in which these changes effect adaptive and maladaptive responses of the heart. This article is part of a Special Issue entitled "Focus on Cardiac Metabolism".

Indexed as

Adaptation, BiologicalGene Expression RegulationStress, PhysiologicalAnimalsHumansMyocardiumProtein BiosynthesisRNA Processing, Post-TranscriptionalTranscription FactorsTranscription Factors

Identifiers

PMID22728216
PMCPMC3474866

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.