Evidence map›Paper›PMID 28236380›Full record

ReviewDiabetes & metabolism journal2017

My Sweetheart Is Broken: Role of Glucose in Diabetic Cardiomyopathy.

Manoja K Brahma, Mark E Pepin, Adam R Wende

Open access · goldAbstract readReview
In one paragraph

Review in Diabetes & metabolism journal, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
7.9field-weighted citation impact, top 2% 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

32 citing papers in PubMed, 1 synthesis or guideline pooled it, 54 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Recent advances associated with cardiometabolic remodeling in diabetes-induced heart failure.American journal of physiology. Heart and circulatory physiology · 2024
    Review
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  12. The role of CD36 in cardiovascular disease.Cardiovascular research · 2022
    Review
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  20. Re-balancing cellular energy substrate metabolism to mend the failing heart.Biochimica et biophysica acta. Molecular basis of disease · 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

3 authors at 1 institution in 1 country.

Manoja K BrahmaDivision of Molecular and Cellular Pathology, Department of Pathology, The University of Alabama at Birmingham, Birmingham, AL, USA.
Mark E PepinDivision of Molecular and Cellular Pathology, Department of Pathology, The University of Alabama at Birmingham, Birmingham, AL, USA.
Adam R WendeDivision of Molecular and Cellular Pathology, Department of Pathology, The University of Alabama at Birmingham, Birmingham, AL, USA. adamwende@uabmc.edu.ORCID http://orcid.org/0000-0002-5536-4675
University of Alabama at Birmingham · US

Funding

University of Alabama at Birmingham's Diabetes Research CenterP30DK079626 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI Kirk Michael Habegger · 2013 to 2026
$19.5M
Interdisciplinary Training in Pathobiology and Rehabilitation Medicine.T32HD071866 · NICHD · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI JAMES RIMMER, Anna E. Thalacker-Mercer · 2012 to 2026
$4.8M
Glucose-Mediated Remodeling of Cardiac DNA MethylationR01HL133011 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI WENDE, ADAM RAYMOND · 2017 to 2020
$1.5M
Mechanisms of glucose mediated cardiac mitochondrial dysfunctionR00HL111322 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI WENDE, ADAM RAYMOND · 2013 to 2015
$870k
Glucose-Mediated Remodeling of Cardiac DNA MethylationR56HL133011 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI WENDE, ADAM RAYMOND · 2016 to 2016
$368k
NHLBI NIH HHS R00 HL111322NHLBI NIH HHS R01 HL133011NHLBI NIH HHS R56 HL133011NICHD NIH HHS T32 HD071866NIDDK NIH HHS P30 DK079626
6 · The paper itself

Abstract

Despite overall reductions in heart disease prevalence, the risk of developing heart failure has remained 2-fold greater among people with diabetes. Growing evidence has supported that fluctuations in glucose level and uptake contribute to cardiovascular disease (CVD) by modifying proteins, DNA, and gene expression. In the case of glucose, clinical studies have shown that increased dietary sugars for healthy individuals or poor glycemic control in diabetic patients further increased CVD risk. Furthermore, even after decades of maintaining tight glycemic control, susceptibility to disease progression can persist following a period of poor glycemic control through a process termed "glycemic memory." In response to chronically elevated glucose levels, a number of studies have identified molecular targets of the glucose-mediated protein posttranslational modification by the addition of an O-linked N-acetylglucosamine to impair contractility, calcium sensitivity, and mitochondrial protein function. Additionally, elevated glucose contributes to dysfunction in coupling glycolysis to glucose oxidation, pentose phosphate pathway, and polyol pathway. Therefore, in the "sweetened" environment associated with hyperglycemia, there are a number of pathways contributing to increased susceptibly to "breaking" the heart of diabetics. In this review we will discuss the unique contribution of glucose to heart disease and recent advances in defining mechanisms of action.

Indexed as

CardiomyopathiesDiabetesGlucoseMetabolism

Identifiers

PMID28236380
PMCPMC5328690
OpenAlexW2550251732

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.