Evidence map›Paper›PMID 26756635›Full record

ReviewComprehensive Physiology2015

Glucose Transporters in Cardiac Metabolism and Hypertrophy.

Dan Shao, Rong Tian

Abstract readReview
In one paragraph

Review in Comprehensive Physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 165 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
165citing 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

165 citing papers in PubMed, 2 syntheses or guidelines pooled it, 241 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Review
  5. Article
  6. Review
  7. Review
  8. Review
  9. Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Review

105 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 at 1 institution in 1 country.

Dan ShaoMitochondria and Metabolism Center, University of Washington, Seattle, Washington, USA.
Rong TianMitochondria and Metabolism Center, University of Washington, Seattle, Washington, USA.
University of Washington · US

Funding

NAD+/NADH ratio, protein acetylation and mitochondrial functionR01HL110349 · NHLBI · UNIVERSITY OF WASHINGTON · PI TIAN, RONG · 2011 to 2020
$5.7M
Isoform-specific function of y-AMPK in the heart.R01HL088634 · NHLBI · UNIVERSITY OF WASHINGTON · PI TIAN, RONG · 2007 to 2015
$3.7M
Glucose And BCAA Metabolism in the HeartR01HL118989 · NHLBI · UNIVERSITY OF WASHINGTON · PI TIAN, RONG · 2014 to 2017
$3.1M
NHLBI NIH HHS HL-088634NHLBI NIH HHS HL-110349NHLBI NIH HHS HL-118989NHLBI NIH HHS R01 HL088634NHLBI NIH HHS R01 HL110349NHLBI NIH HHS R01 HL118989
6 · The paper itself

Abstract

The heart is adapted to utilize all classes of substrates to meet the high-energy demand, and it tightly regulates its substrate utilization in response to environmental changes. Although fatty acids are known as the predominant fuel for the adult heart at resting stage, the heart switches its substrate preference toward glucose during stress conditions such as ischemia and pathological hypertrophy. Notably, increasing evidence suggests that the loss of metabolic flexibility associated with increased reliance on glucose utilization contribute to the development of cardiac dysfunction. The changes in glucose metabolism in hypertrophied hearts include altered glucose transport and increased glycolysis. Despite the role of glucose as an energy source, changes in other nonenergy producing pathways related to glucose metabolism, such as hexosamine biosynthetic pathway and pentose phosphate pathway, are also observed in the diseased hearts. This article summarizes the current knowledge regarding the regulation of glucose transporter expression and translocation in the heart during physiological and pathological conditions. It also discusses the signaling mechanisms governing glucose uptake in cardiomyocytes, as well as the changes of cardiac glucose metabolism under disease conditions.

Indexed as

AnimalsCardiomegalyGlucoseGlucose Transport Proteins, FacilitativeHumansMyocardiumGlucoseGlucose Transport Proteins, Facilitative

Identifiers

PMID26756635
PMCPMC4760112
OpenAlexW2417223785

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.