Evidence map›Paper›PMID 20201903›Full record

ReviewAnnals of the New York Academy of Sciences2010

Return to the fetal gene program: a suggested metabolic link to gene expression in the heart.

Heinrich Taegtmeyer, Shiraj Sen, Deborah Vela

Abstract readReview
In one paragraph

Review in Annals of the New York Academy of Sciences, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 242 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
242citing papers in PubMed, 2 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

242 citing papers in PubMed, 2 syntheses or guidelines pooled it.

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182 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

3 authors.

Heinrich TaegtmeyerThe University of Texas-Houston Medical School, Department of Internal Medicine, Division of Cardiology, Houston, Texas 77030, USA. Heinrich.Taegtmeyer@uth.tmc.edu
Shiraj Sen
Deborah Vela

Funding

SWITCHING OF METABOLIC GENES IN UNLOADED HEARTR01HL061483 · NHLBI · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI TAEGTMEYER, HEINRICH · 1999 to 2021
$6.2M
NHLBI NIH HHS R01 HL061483NIA NIH HHS R01 HL/AG 61483
6 · The paper itself

Abstract

A hallmark of cardiac metabolism before birth is the predominance of carbohydrate use for energy provision. After birth, energy substrate metabolism rapidly switches to the oxidation of fatty acids. This switch accompanies the expression of "adult" isoforms of metabolic enzymes and other proteins. However, in a variety of pathophysiologic conditions, including hypoxia, ischemia, hypertrophy, atrophy, diabetes, and hypothyroidism, the postnatal heart returns to the "fetal" gene program. These adaptive mechanisms are also a feature of the failing heart muscle, where at a certain point this fetal-like reprogramming no longer suffices to support cardiac structure and function. We advance the hypothesis that in the postnatal heart, metabolic remodeling triggers the process through glycosylation of transcription factors, potentially protecting the stressed heart from irreversible functional impairment and programmed cell death. In other words, we propose a metabolic link to gene expression in the heart.

Indexed as

Gene Expression RegulationAnimalsApoptosisGlucoseHeart DiseasesHumansMyocardiumStress, PhysiologicalGlucose

Identifiers

PMID20201903
PMCPMC3625436

What OpenQuestion holds

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Registered trials

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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.