Evidence map›Paper›PMID 27166197›Full record

ReviewBiochimica et biophysica acta2016

Cellular mechanisms and consequences of glycation in atherosclerosis and obesity.

Raquel López-Díez, Alexander Shekhtman, Ravichandran Ramasamy, Ann Marie Schmidt

Abstract readReview
In one paragraph

Review in Biochimica et biophysica acta, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
–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

34 citing papers in PubMed.

  1. Trial
  2. The interaction between dysfunction of vasculature and tauopathy in Alzheimer's disease and related dementias.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Review
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  15. An in Silico Approach Reveals the Potential Function of Cyanidin-3-o-glucoside of Red Rice in Inhibiting the Advanced Glycation End Products (AGES)-Receptor (RAGE) Signaling Pathway.Acta informatica medica : AIM : journal of the Society for Medical Informatics of Bosnia & Herzegovina : casopis Drustva za medicinsku informatiku BiH · 2020
    Article
  16. Review
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  19. S100 proteins in obesity: liaisons dangereuses.Cellular and molecular life sciences : CMLS · 2020
    Review
  20. Article
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

4 authors.

Raquel López-DíezDiabetes Research Program, Division of Endocrinology, Department of Medicine, NYU Langone Medical Center, New York, NY 10016, United States.
Alexander ShekhtmanDepartment of Chemistry, University at Albany, State University of New York, 1400 Washington Avenue, Albany, NY 12222, United States.
Ravichandran RamasamyDiabetes Research Program, Division of Endocrinology, Department of Medicine, NYU Langone Medical Center, New York, NY 10016, United States.
Ann Marie SchmidtDiabetes Research Program, Division of Endocrinology, Department of Medicine, NYU Langone Medical Center, New York, NY 10016, United States. Electronic address: annmarie.schmidt@nyumc.org.

Funding

Translational Research CoreP30DK020541 · NIDDK · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI STREAMSON C CHUA · 2015 to 2026
$27.7M
VASCULAR AND MONOCYTE DYSFUNCTION IN WOUND REPAIRP01HL060901 · NHLBI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI YAN, SHI FANG · 1999 to 2017
$20.2M
Targeting RAGE-mDia1 in Diabetic Complications: Mechanisms and TherapeuticsR24DK103032 · NIDDK · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI RAMASAMY, RAVICHANDRAN, SCHMIDT, ANN MARIE · 2014 to 2018
$4.2M
RAGE, Macrophages & HDL BiologyR01HL118565 · NHLBI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI SCHMIDT, ANN MARIE · 2013 to 2017
$2.1M
NHLBI NIH HHS P01 HL060901NHLBI NIH HHS R01 HL118565NIDDK NIH HHS P30 DK020541NIDDK NIH HHS R24 DK103032
6 · The paper itself

Abstract

Post-translational modification of proteins imparts diversity to protein functions. The process of glycation represents a complex set of pathways that mediates advanced glycation endproduct (AGE) formation, detoxification, intracellular disposition, extracellular release, and induction of signal transduction. These processes modulate the response to hyperglycemia, obesity, aging, inflammation, and renal failure, in which AGE formation and accumulation is facilitated. It has been shown that endogenous anti-AGE protective mechanisms are thwarted in chronic disease, thereby amplifying accumulation and detrimental cellular actions of these species. Atop these considerations, receptor for advanced glycation endproducts (RAGE)-mediated pathways downregulate expression and activity of the key anti-AGE detoxification enzyme, glyoxalase-1 (GLO1), thereby setting in motion an interminable feed-forward loop in which AGE-mediated cellular perturbation is not readily extinguished. In this review, we consider recent work in the field highlighting roles for glycation in obesity and atherosclerosis and discuss emerging strategies to block the adverse consequences of AGEs. This article is part of a Special Issue entitled: The role of post-translational protein modifications on heart and vascular metabolism edited by Jason R.B. Dyck & Jan F.C. Glatz.

Indexed as

Protein Processing, Post-TranslationalAnimalsAtherosclerosisChronic DiseaseGlycation End Products, AdvancedHumansLactoylglutathione LyaseObesityReceptor for Advanced Glycation End ProductsAGER protein, humanGLO1 protein, humanGlycation End Products, AdvancedLactoylglutathione LyaseReceptor for Advanced Glycation End ProductsAtherosclerosisDiabetesGlycationObesityReceptor for advanced glycation end productsTheraepeutics

Identifiers

PMID27166197
PMCPMC5101176

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.