Evidence mapPaperPMID 34422213Full record

ArticleOxidative medicine and cellular longevity2021

In Vitro Evaluation of the Toxicological Profile and Oxidative Stress of Relevant Diet-Related Advanced Glycation End Products and Related 1,2-Dicarbonyls.

Vanesa Cepas, Friederike Manig, Juan C Mayo, Michael Hellwig, Debora Collotta, Valentina Sanmartino, Rebeca Carrocera-Pumarino, Massimo Collino, Thomas Henle, Rosa M Sainz

Open access · hybridAbstract readEvaluation Study
In one paragraph

Article in Oxidative medicine and cellular longevity, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

8 citing papers in PubMed, 22 citations in OpenAlex.

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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

10 authors at 3 institutions in 3 countries.

Vanesa CepasDepartamento de Morfología y Biología Celular, Universidad de Oviedo, Spain.ORCID https://orcid.org/0000-0003-0839-4369
Friederike ManigChair of Food Chemistry, Technische Universität Dresden, D-01062 Dresden, Germany.ORCID https://orcid.org/0000-0003-3331-7816
Juan C MayoDepartamento de Morfología y Biología Celular, Universidad de Oviedo, Spain.ORCID https://orcid.org/0000-0002-0882-2047
Michael HellwigChair of Food Chemistry, Technische Universität Dresden, D-01062 Dresden, Germany.ORCID https://orcid.org/0000-0001-8528-6893
Debora CollottaDepartment of Neurosciences 'Rita Levi Montalcini', University of Turin, Italy.ORCID https://orcid.org/0000-0002-5569-7509
Valentina SanmartinoDepartment of Neurosciences 'Rita Levi Montalcini', University of Turin, Italy.
Rebeca Carrocera-PumarinoDepartamento de Morfología y Biología Celular, Universidad de Oviedo, Spain.ORCID https://orcid.org/0000-0002-6690-1026
Massimo CollinoDepartment of Neurosciences 'Rita Levi Montalcini', University of Turin, Italy.ORCID https://orcid.org/0000-0001-8782-3496
Thomas HenleChair of Food Chemistry, Technische Universität Dresden, D-01062 Dresden, Germany.ORCID https://orcid.org/0000-0001-6220-7267
Rosa M SainzDepartamento de Morfología y Biología Celular, Universidad de Oviedo, Spain.ORCID https://orcid.org/0000-0003-3048-5582
Universidad de Oviedo · ESTechnische Universität Dresden · DEUniversity of Turin · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

During food processing and storage, and in tissues and fluids under physiological conditions, the Maillard reaction occurs. During this reaction, reactive 1,2-dicarbonyl compounds arise as intermediates that undergo further reactions to form advanced glycation end products (AGEs). Diet is the primary source of exogenous AGEs. Endogenously formed AGEs have been proposed as a risk factor in the pathogenesis of diet-related diseases such as diabetes, insulin resistance, cardiovascular diseases, or chronic disease. AGEs may differently contribute to the diet-related exacerbation of oxidative stress, inflammation, and protein modifications. Here, to understand the contribution of each compound, we tested individually, for the first time, the effect of five 1,2-dicarbonyl compounds 3-deoxyglucosone (3-DG), 3-deoxygalactosone (3-DGal), 3,4-dideoxyglucosone-3-ene (3,4-DGE), glyoxal (GO), and methylglyoxal (MGO) and four different glycated amino acids N-

Indexed as

ApoptosisDeoxyglucoseGalactoseGlycation End Products, AdvancedHumansInflammationIn Vitro TechniquesKeratinocytesNF-kappa BNLR Family, Pyrin Domain-Containing 3 ProteinOxidative StressPyronesReactive Oxygen Species3,4-dideoxyglucosone-3-ene3-deoxygalactosone3-deoxyglucosoneDeoxyglucoseGalactoseGlycation End Products, AdvancedNF-kappa BNLR Family, Pyrin Domain-Containing 3 ProteinNLRP3 protein, humanPyronesReactive Oxygen Species

Identifiers

PMID34422213
PMCPMC8371648
OpenAlexW3189272718

What Socratic 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 Socratic graph.