Evidence map›Paper›PMID 32014551›Full record

ReviewBiochimica et biophysica acta. Molecular basis of disease2020

Regulation of cardiac O-GlcNAcylation: More than just nutrient availability.

Helen E Collins, John C Chatham

Open access · greenAbstract readReview
In one paragraph

Review in Biochimica et biophysica acta. Molecular basis of disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

21 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. PERM1 regulates mitochondrial energetics through O-GlcNAcylation in the heart.Journal of molecular and cellular cardiology · 2025
    Article
  6. Article
  7. Proteomics of the heart.Physiological reviews · 2024
    Review
  8. Article
  9. Review
  10. Review
  11. Review
  12. Article
  13. Reduced O-GlcNAcylation diminishes cardiomyocyte CaJournal of molecular and cellular cardiology · 2023
    Article
  14. Article
  15. Review
  16. Enhancement ofMolecules (Basel, Switzerland) · 2021
    Article
  17. Article
  18. Review
  19. Review
  20. Glucose transporters in cardiovascular system in health and disease.Pflugers Archiv : European journal of physiology · 2020
    Review
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 at 2 institutions in 1 country.

Helen E CollinsDivision of Environmental Medicine, Department of Medicine, University of Louisville, Louisville, KY, United States of America.
John C ChathamDivision of Molecular and Cellular Pathology, Department of Pathology, University of Alabama at Birmingham, Birmingham, AL, United States of America. Electronic address: jchatham@uabmc.edu.
University of Alabama at Birmingham · USUniversity of Louisville · US

Funding

University of Alabama at Birmingham's Diabetes Research CenterP30DK079626 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BARBARA A GOWER · 2013 to 2026
$19.5M
Aberrant Circadian Regulation of Autophagy in the Heart During DiabetesR01HL142216 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI CHATHAM, JOHN C, YOUNG, MARTIN E · 2018 to 2021
$2.3M
Glucose-Mediated Remodeling of Cardiac DNA MethylationR01HL133011 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI WENDE, ADAM RAYMOND · 2017 to 2020
$1.5M
STIM1 mediated calcium entry: A new paradigm of metabolic regulation of cardiomyoR21HL110366 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI CHATHAM, JOHN C · 2012 to 2013
$407k
Glucose-Mediated Remodeling of Cardiac DNA MethylationR56HL133011 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI WENDE, ADAM RAYMOND · 2016 to 2016
$368k
NHLBI NIH HHS R01 HL133011NHLBI NIH HHS R01 HL142216NHLBI NIH HHS R21 HL110366NHLBI NIH HHS R56 HL133011NIDDK NIH HHS P30 DK079626
6 · The paper itself

Abstract

The post-translational modification of serine and threonine residues of nuclear, cytosolic, and mitochondrial proteins by O-linked β-N-acetyl glucosamine (O-GlcNAc) has long been seen as an important regulatory mechanism in the cardiovascular system. O-GlcNAcylation of cardiac proteins has been shown to contribute to the regulation of transcription, metabolism, mitochondrial function, protein quality control and turnover, autophagy, and calcium handling. In the heart, acute increases in O-GlcNAc have been associated with cardioprotection, such as those observed during ischemia/reperfusion. Conversely, chronic increases in O-GlcNAc, often associated with diabetes and nutrient excess, have been shown to contribute to cardiac dysfunction. Traditionally, many studies have linked changes in O-GlcNAc with nutrient availability and as such O-GlcNAcylation is often seen as a nutrient driven process. However, emerging evidence suggests that O-GlcNAcylation may also be regulated by non-nutrient dependent mechanisms, such as transcriptional and post-translational regulation. Therefore, the goals of this review are to provide an overview of the impact of O-GlcNAcylation in the cardiovascular system, how this is regulated and to discuss the emergence of regulatory mechanisms other than nutrient availability.

Indexed as

AcetylglucosamineAnimalsCardiovascular DiseasesDisease Models, AnimalFeeding BehaviorHeartHumansMyocardiumN-AcetylglucosaminyltransferasesNutrientsProtein Processing, Post-TranslationalStress, PhysiologicalAcetylglucosamineN-AcetylglucosaminyltransferasesNutrientsCardiomyocyteGFATHeartMetabolismNutrient regulationO-GlcNAcO-GlcNAcase (OGA)O-GlcNAc transferase (OGT)

Identifiers

PMID32014551
PMCPMC7703857
OpenAlexW3003674302

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.