Evidence map›Paper›PMID 28212304›Full record

ReviewInternational journal of molecular sciences2017

Methylglyoxal-Derived Advanced Glycation Endproducts in Multiple Sclerosis.

Suzan Wetzels, Kristiaan Wouters, Casper G Schalkwijk, Tim Vanmierlo, Jerome J A Hendriks

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

42 citing papers in PubMed, 79 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Article
  5. Effect of Glyoxal on Plasma Membrane and Cytosolic Proteins of Erythrocytes.International journal of molecular sciences · 2025
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Highly specific σProceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  15. Article
  16. Review
  17. Highly specific σbioRxiv : the preprint server for biology · 2023
    Article
  18. Article
  19. Review
  20. 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

5 authors at 2 institutions in 2 countries.

Suzan WetzelsDepartment of Internal Medicine, Cardiovascular Research Institute Maastricht, Maastricht University, 6229 Maastricht, The Netherlands. suzan.wetzels@uhasselt.be.
Kristiaan WoutersDepartment of Internal Medicine, Cardiovascular Research Institute Maastricht, Maastricht University, 6229 Maastricht, The Netherlands. kristiaan.wouters@maastrichtuniversity.nl.
Casper G SchalkwijkDepartment of Internal Medicine, Cardiovascular Research Institute Maastricht, Maastricht University, 6229 Maastricht, The Netherlands. c.schalkwijk@maastrichtuniversity.nl.
Tim VanmierloDepartment of Immunology and Biochemistry, Biomedical Research Institute, Hasselt University, Martelarenlaan 42, 3500 Hasselt, Belgium. tim.vanmierlo@uhasselt.be.
Jerome J A HendriksDepartment of Immunology and Biochemistry, Biomedical Research Institute, Hasselt University, Martelarenlaan 42, 3500 Hasselt, Belgium. jerome.hendriks@uhasselt.be.
Maastricht University · NLHasselt University · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multiple sclerosis (MS) is a demyelinating disease of the central nervous system (CNS). The activation of inflammatory cells is crucial for the development of MS and is shown to induce intracellular glycolytic metabolism in pro-inflammatory microglia and macrophages, as well as CNS-resident astrocytes. Advanced glycation endproducts (AGEs) are stable endproducts formed by a reaction of the dicarbonyl compounds methylglyoxal (MGO) and glyoxal (GO) with amino acids in proteins, during glycolysis. This suggests that, in MS, MGO-derived AGEs are formed in glycolysis-driven cells. MGO and MGO-derived AGEs can further activate inflammatory cells by binding to the receptor for advanced glycation endproducts (RAGE). Recent studies have revealed that AGEs are increased in the plasma and brain of MS patients. Therefore, AGEs might contribute to the inflammatory status in MS. Moreover, the main detoxification system of dicarbonyl compounds, the glyoxalase system, seems to be affected in MS patients, which may contribute to high MGO-derived AGE levels. Altogether, evidence is emerging for a contributing role of AGEs in the pathology of MS. In this review, we provide an overview of the current knowledge on the involvement of AGEs in MS.

Indexed as

Adaptive ImmunityAnimalsGlycation End Products, AdvancedGlycolysisHumansImmunity, InnateLipid PeroxidationMultiple SclerosisOxidation-ReductionOxidative StressPyruvaldehydeReceptor for Advanced Glycation End ProductsGlycation End Products, AdvancedPyruvaldehydeReceptor for Advanced Glycation End Productsadvanced glycation endproductsglyoxalase systemmethylglyoxalmultiple sclerosisreceptor for advanced glycation endproduct

Identifiers

PMID28212304
PMCPMC5343955
OpenAlexW2587838788

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.