Evidence map›Paper›PMID 26788516›Full record

ArticleJournal of diabetes research2016

Expression of the Receptor for Advanced Glycation End Products in Epicardial Fat: Link with Tissue Thickness and Local Insulin Resistance in Coronary Artery Disease.

Elena Dozio, Elena Vianello, Silvia Briganti, John Lamont, Lorenza Tacchini, Gerd Schmitz, Massimiliano Marco Corsi Romanelli

Open access · goldAbstract read
In one paragraph

Article in Journal of diabetes research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 17% 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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.

  1. Pooled it
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  6. Unraveling the Roles of HIF-1, HO-1, GLUT-1 and GLUT-4 in Myocardial Protection.International journal of drug discovery and pharmacology · 2024
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  10. Epicardial adipose tissue in contemporary cardiology.Nature reviews. Cardiology · 2022 · on this map
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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

7 authors at 4 institutions in 3 countries.

Elena DozioDepartment of Biomedical Sciences for Health, University of Milan, Via L. Mangiagalli 31, 20133 Milan, Italy.
Elena VianelloDepartment of Biomedical Sciences for Health, University of Milan, Via L. Mangiagalli 31, 20133 Milan, Italy.
Silvia BrigantiDiabetology and Metabolic Disease Unit, I.R.C.C.S. Policlinico San Donato, Piazza E. Malan 1, 20097 San Donato Milanese, Italy.
John LamontRandox Laboratories Ltd., R&D, 55 Diamond Road, Crumlin, Antrim, Belfast BT29 4QY, UK.
Lorenza TacchiniDepartment of Biomedical Sciences for Health, University of Milan, Via L. Mangiagalli 31, 20133 Milan, Italy.
Gerd SchmitzInstitute for Clinical Chemistry and Laboratory Medicine, University of Regensburg, Universitätsstraße 31, 93053 Regensburg, Germany.
Massimiliano Marco Corsi RomanelliDepartment of Biomedical Sciences for Health, University of Milan, Via L. Mangiagalli 31, 20133 Milan, Italy; Service of Laboratory Medicine 1-Clinical Pathology, I.R.C.C.S. Policlinico San Donato, Piazza E. Malan 1, 20097 San Donato Milanese, Italy.
University of Milan · ITIRCCS Policlinico San Donato · ITRandox (United Kingdom) · GBUniversity of Regensburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Increased expression of receptor for advanced glycation end products (RAGE) in adipose tissue has been associated with inflammation, adipocyte hypertrophy, and impaired insulin signal. Epicardial adipose tissue (EAT), a visceral fat surrounding the myocardium, is potentially involved in the onset/progression of coronary artery disease (CAD). To date, the role of RAGE in EAT has not been explored much. We examined whether the RAGE expression in EAT was associated with EAT adiposity and metabolic dysfunctions normally found in CAD patients. EAT samples were obtained from 33 patients undergoing open-heart surgery. EAT expression of RAGE, GLUT4, adiponenctin, GLO1, HMGB1, TLR-4, and MyD88 was analyzed by microarray. EAT thickness was quantified by echocardiography. Anthropometric measures and clinical parameters were taken. BMI, HOMA-IR, and LAP indices were calculated. With increasing RAGE expression in EAT we observed increases in EAT thickness, reduced expression of GLUT4, adiponectin, and GLO1, and elevations of HMGB1, TLR-4, and MyD88. There were significant correlations between RAGE and EAT thickness and between RAGE and the genes. LAP was higher in patients with increased RAGE expression. Our data suggest that in CAD patients RAGE may be involved in promoting EAT adiposity and metabolic dysfunction, such as impaired insulin signaling.

Indexed as

AdiposityInsulin ResistanceAgedAged, 80 and overCoronary Artery DiseaseHMGB1 ProteinHumansIntra-Abdominal FatLactoylglutathione LyaseMaleMiddle AgedMyeloid Differentiation Factor 88PericardiumReceptor for Advanced Glycation End ProductsToll-Like Receptor 4UltrasonographyAGER protein, humanGLO1 protein, humanHMGB1 ProteinHMGB1 protein, humanLactoylglutathione LyaseMYD88 protein, humanMyeloid Differentiation Factor 88Receptor for Advanced Glycation End ProductsTLR4 protein, humanToll-Like Receptor 4

Identifiers

PMID26788516
PMCPMC4691615
OpenAlexW1535355536

What OpenQuestion holds

Textmetadata
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.