Evidence map›Paper›PMID 33883682›Full record

ArticleScientific reports2021

GLUT1 overexpression enhances glucose metabolism and promotes neonatal heart regeneration.

Viviana M Fajardo, Iris Feng, Bao Ying Chen, Cesar A Perez-Ramirez, Baochen Shi, Peter Clark, Rong Tian, Ching-Ling Lien, Matteo Pellegrini, Heather Christofk and 2 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
3.3field-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

45 citing papers in PubMed, 56 citations in OpenAlex.

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  5. Signaling pathways regulating cardiac regeneration.Cell regeneration (London, England) · 2026
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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

12 authors at 3 institutions in 1 country.

Viviana M FajardoDivision of Neonatology, Department of Pediatrics, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA, USA.
Iris FengDepartment of Molecular, Cell, Developmental Biology, School of Life Science, University of California Los Angeles, Los Angeles, CA, USA.
Bao Ying ChenDepartment of Molecular and Medical Pharmacology, University of California, Los Angeles, Los Angeles, CA, USA.
Cesar A Perez-RamirezDepartment of Biological Chemistry, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA, USA.
Baochen ShiDepartment of Molecular, Cell, Developmental Biology, School of Life Science, University of California Los Angeles, Los Angeles, CA, USA.
Peter ClarkDepartment of Molecular and Medical Pharmacology, University of California, Los Angeles, Los Angeles, CA, USA.
Rong TianDepartment of Anesthesiology and Pain Medicine, University of Washington, Seattle, WA, USA.
Ching-Ling LienThe Saban Research Institute of Children's Hospital Los Angeles, Los Angeles, CA, USA.
Matteo PellegriniDepartment of Molecular, Cell, Developmental Biology, School of Life Science, University of California Los Angeles, Los Angeles, CA, USA.
Heather ChristofkDepartment of Biological Chemistry, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA, USA.
Haruko NakanoDepartment of Molecular, Cell, Developmental Biology, School of Life Science, University of California Los Angeles, Los Angeles, CA, USA.
Atsushi NakanoDepartment of Molecular, Cell, Developmental Biology, School of Life Science, University of California Los Angeles, Los Angeles, CA, USA. anakano@ucla.edu.
University of California, Los Angeles · USUniversity of Southern California · USUniversity of Washington · US

Funding

UCLA Child Health Research Career Development AwardK12HD034610 · NICHD · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI DEVASKAR, SHERIN U · 2002 to 2017
$6.6M
Nutrient Regulation of Cancer Cell GrowthR01CA215185 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Heather Christofk · 2018 to 2026
$4.3M
Mitochondrial function and glycolytic switch in pathological cardiac hypertrophyR01HL142628 · NHLBI · UNIVERSITY OF WASHINGTON · PI TIAN, RONG · 2018 to 2021
$2.4M
Cxc12 chemokine signaling regulates synchronous development of coronary vessels and myocardiumR01HL130172 · NHLBI · CHILDREN'S HOSPITAL OF LOS ANGELES · PI LIEN, CHING-LING E · 2017 to 2020
$1.7M
Metabolic regulation of heart formationR01HL142801 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI NAKANO, ATSUSHI · 2019 to 2022
$1.6M
NCI NIH HHS R01 CA215185NHLBI NIH HHS R01 HL130172NHLBI NIH HHS R01 HL142628NHLBI NIH HHS R01 HL142801NICHD NIH HHS K12 HD034610
6 · The paper itself

Abstract

The mammalian heart switches its main metabolic substrate from glucose to fatty acids shortly after birth. This metabolic switch coincides with the loss of regenerative capacity in the heart. However, it is unknown whether glucose metabolism regulates heart regeneration. Here, we report that glucose metabolism is a determinant of regenerative capacity in the neonatal mammalian heart. Cardiac-specific overexpression of Glut1, the embryonic form of constitutively active glucose transporter, resulted in an increase in glucose uptake and concomitant accumulation of glycogen storage in postnatal heart. Upon cryoinjury, Glut1 transgenic hearts showed higher regenerative capacity with less fibrosis than non-transgenic control hearts. Interestingly, flow cytometry analysis revealed two distinct populations of ventricular cardiomyocytes: Tnnt2-high and Tnnt2-low cardiomyocytes, the latter of which showed significantly higher mitotic activity in response to high intracellular glucose in Glut1 transgenic hearts. Metabolic profiling shows that Glut1-transgenic hearts have a significant increase in the glucose metabolites including nucleotides upon injury. Inhibition of the nucleotide biosynthesis abrogated the regenerative advantage of high intra-cardiomyocyte glucose level, suggesting that the glucose enhances the cardiomyocyte regeneration through the supply of nucleotides. Our data suggest that the increase in glucose metabolism promotes cardiac regeneration in neonatal mouse heart.

Indexed as

RegenerationAnimalsAnimals, NewbornFemaleGlucoseGlucose Transporter Type 1HeartMaleMetabolomicsMiceMice, Inbred ICRMice, TransgenicMyocytes, CardiacNucleotidesGlucoseGlucose Transporter Type 1NucleotidesSlc2a1 protein, mouse

Identifiers

PMID33883682
PMCPMC8060418
OpenAlexW3152515249

What OpenQuestion holds

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LicenceCC BY
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.