Evidence map›Paper›PMID 25791172›Full record

ReviewCardiology2015

Remodeling of glucose metabolism precedes pressure overload-induced left ventricular hypertrophy: review of a hypothesis.

Bijoy K Kundu, Min Zhong, Shiraj Sen, Giovanni Davogustto, Susanna R Keller, Heinrich Taegtmeyer

Abstract readReview
In one paragraph

Review in Cardiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed, 1 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

66 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Review
  4. Qianyang Yuyin granule modulates glycolysis and inflammatory response to treat hypertensive cardiac remodeling.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2026
    Article
  5. Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. UCP1-dependent brown adipose activation accelerates cardiac metabolic remodeling and reduces initial hypertrophic and fibrotic responses to pathological stress.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
    Article
  17. Article
  18. Article
  19. Article
  20. Article

6 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

6 authors.

Bijoy K KunduDepartment of Radiology and Medical Imaging, University of Virginia, Charlottesville, Va., USA.
Min Zhong
Shiraj Sen
Giovanni Davogustto
Susanna R Keller
Heinrich Taegtmeyer

Funding

SWITCHING OF METABOLIC GENES IN UNLOADED HEARTR01HL061483 · NHLBI · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI TAEGTMEYER, HEINRICH · 1999 to 2021
$6.2M
Metabolic remodeling precedes and triggers left ventricular remodeling in cardiacR21HL102627 · NHLBI · UNIVERSITY OF VIRGINIA · PI KUNDU, BIJOY K · 2010 to 2011
$408k
NHLBI NIH HHS HL R01-61483NHLBI NIH HHS HL R21-102627NHLBI NIH HHS R01 HL061483NHLBI NIH HHS R21 HL102627
6 · The paper itself

Abstract

When subjected to pressure overload, the ventricular myocardium shifts from fatty acids to glucose as its main source for energy provision and frequently increases its mass. Here, we review the evidence in support of the concept that metabolic remodeling, measured as an increased myocardial glucose uptake using dynamic positron emission tomography (PET) with the glucose analogue 2-deoxy-2-[(18)F]fluoro-D-glucose (FDG), precedes the onset of left ventricular hypertrophy (LVH) and heart failure. Consistent with this, early intervention with propranolol, which attenuates glucose uptake, prevents the maladaptive metabolic response and preserves cardiac function in vivo. We also review ex vivo studies suggesting a link between dysregulated myocardial glucose metabolism, intracellular accumulation of glucose 6-phosphate (G6P) and contractile dysfunction of the heart. G6P levels correlate with activation of mTOR (mechanistic target of rapamycin) and endoplasmic reticulum stress. This sequence of events could be prevented by pretreatment with rapamycin (mTOR inhibition) or metformin (enzyme 5'-AMP-activated protein kinase activation). In conclusion, we propose that metabolic imaging with FDG PET may provide a novel approach to guide the treatment of patients with hypertension-induced LVH.

Indexed as

3-O-MethylglucoseAnimalsDisease Models, AnimalEndoplasmic Reticulum StressFatty AcidsGlucose-6-PhosphateHeart FailureHeart VentriclesHumansHypertensionHypertrophy, Left VentricularHypoglycemic AgentsMetforminMiceMyocardiumPositron-Emission Tomography2-deoxy-2-fluoro-3-O-methylglucose3-O-MethylglucoseFatty AcidsGlucose-6-PhosphateHypoglycemic AgentsMetforminSirolimusTOR Serine-Threonine Kinases

Identifiers

PMID25791172
PMCPMC4394867

What OpenQuestion holds

Texttitle and abstract
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.