Evidence map›Paper›PMID 27277623›Full record

ReviewGlycoconjugate journal2016

Implication of advanced glycation end products (Ages) and their receptor (Rage) on myocardial contractile and mitochondrial functions.

Remi Neviere, Yichi Yu, Lei Wang, Frederic Tessier, Eric Boulanger

Abstract readReview
PubMed Publisher
In one paragraph

Review in Glycoconjugate journal, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.5field-weighted citation impact, top 8% 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, 47 citations in OpenAlex.

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  12. Integrative Role of Albumin: Evolutionary, Biochemical and Pathophysiological Aspects.Journal of evolutionary biochemistry and physiology · 2021
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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

5 authors at 4 institutions in 2 countries.

Remi NeviereDepartment of Physiology, School of Medicine, Pole Recherche 1, place de Verdun, 59045, Lille Cedex, France. rneviere@univ-lille2.fr.
Yichi YuLIRIC INSERM U995/Team "Glycation: from inflammation to aging", Lille University, Villeneuve d'Ascq, France.
Lei WangLIRIC INSERM U995/Team "Glycation: from inflammation to aging", Lille University, Villeneuve d'Ascq, France.
Frederic TessierLIRIC INSERM U995/Team "Glycation: from inflammation to aging", Lille University, Villeneuve d'Ascq, France.
Eric BoulangerLIRIC INSERM U995/Team "Glycation: from inflammation to aging", Lille University, Villeneuve d'Ascq, France.
Lille Inflammation Research International Center · FRInserm · FRShanghai Jiao Tong University · CNUniversité de Lille · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Advanced glycation end products (AGEs) play an important role for the development and/or progression of cardiovascular diseases, mainly through induction of oxidative stress and inflammation. AGEs are a heterogeneous group of molecules formed by non-enzymatic reaction of reducing sugars with amino acids of proteins, lipids and nucleic acids. AGEs are mainly formed endogenously, while recent studies suggest that diet constitutes an important exogenous source of AGEs. The presence and accumulation of AGEs in various cardiac cell types affect extracellular and intracellular structure and function. AGEs contribute to a variety of microvascular and macrovascular complications through the formation of cross-links between molecules in the basement membrane of the extracellular matrix and by engaging the receptor for advanced glycation end products (RAGE). Activation of RAGE by AGEs causes up regulation of the transcription factor nuclear factor-κB and its target genes. of the RAGE engagement stimulates oxidative stress, evokes inflammatory and fibrotic reactions, which all contribute to the development and progression of devastating cardiovascular disorders. This review discusses potential targets of glycation in cardiac cells, and underlying mechanisms that lead to heart failure with special interest on AGE-induced mitochondrial dysfunction in the myocardium.

Indexed as

Cardiovascular DiseasesMyocardial ContractionGlycation End Products, AdvancedHumansMitochondria, HeartMyocardiumOxidative StressReceptor for Advanced Glycation End ProductsAGER protein, humanGlycation End Products, AdvancedReceptor for Advanced Glycation End ProductsAdvanced glycation end productsCardiovascularMitochondriaSignaling pathways

Identifiers

PMID27277623
OpenAlexW2409031417

What OpenQuestion holds

Textmetadata
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.