Evidence map›Paper›PMID 27406712›Full record

ReviewGlycoconjugate journal2016

Dicarbonyls and glyoxalase in disease mechanisms and clinical therapeutics.

Naila Rabbani, Mingzhan Xue, Paul J Thornalley

Open access · hybridAbstract readReview
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 89 papers.

0numbers the graph read from it
0cells of the map it votes in
89citing papers in PubMed
13.2field-weighted citation impact, top 1% 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

89 citing papers in PubMed, 161 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Deciphering the mechanisms by which probioticCurrent research in food science · 2026
    Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Methylglyoxal Formation-Metabolic Routes and Consequences.Antioxidants (Basel, Switzerland) · 2025
    Review
  15. Review
  16. Dual roles of methylglyoxal in cancer.Frontiers in oncology · 2025
    Review
  17. Article
  18. Article
  19. Article
  20. Article

29 more citing papers are in PubMed but not listed here.

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

3 authors at 2 institutions in 1 country.

Naila RabbaniWarwick Systems Biology Centre, Coventry House, University of Warwick, Coventry, CV4 7AL, UK.
Mingzhan XueGlyoxalase Research Group, Clinical Sciences Research Laboratories, Warwick Medical School, University of Warwick, University Hospital, Coventry, CV2 2DX, UK.
Paul J ThornalleyWarwick Systems Biology Centre, Coventry House, University of Warwick, Coventry, CV4 7AL, UK. P.J.Thornalley@warwick.ac.uk.
University of Warwick · GBUniversity Hospital Coventry · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The reactive dicarbonyl metabolite methylglyoxal (MG) is the precursor of the major quantitative advanced glycation endproducts (AGEs) in physiological systems - arginine-derived hydroimidazolones and deoxyguanosine-derived imidazopurinones. The glyoxalase system in the cytoplasm of cells provides the primary defence against dicarbonyl glycation by catalysing the metabolism of MG and related reactive dicarbonyls. Dicarbonyl stress is the abnormal accumulation of dicarbonyl metabolites leading to increased protein and DNA modification contributing to cell and tissue dysfunction in ageing and disease. It is produced endogenously by increased formation and/or decreased metabolism of dicarbonyl metabolites. Dicarbonyl stress contributes to ageing, disease and activity of cytotoxic chemotherapeutic agents. It contributes to ageing through age-related decline in glyoxalase 1 (Glo-1) activity. Glo-1 has a dual role in cancer as a tumour suppressor protein prior to tumour development and mediator of multi-drug resistance in cancer treatment, implicating dicarbonyl glycation of DNA in carcinogenesis and dicarbonyl-driven cytotoxicity in mechanism of action of anticancer drugs. Glo-1 is a driver of cardiovascular disease, likely through dicarbonyl stress-driven dyslipidemia and vascular cell dysfunction. Dicarbonyl stress is also a contributing mediator of obesity and vascular complications of diabetes. There are also emerging roles in neurological disorders. Glo-1 responds to dicarbonyl stress to enhance cytoprotection at the transcriptional level through stress-responsive increase of Glo-1 expression. Small molecule Glo-1 inducers are in clinical development for improved metabolic, vascular and renal health and Glo-1 inhibitors in preclinical development for multidrug resistant cancer chemotherapy.

Indexed as

AgingAnimalsDyslipidemiasGlycation End Products, AdvancedHumansLactoylglutathione LyaseNeoplasmsPyruvaldehydeVascular DiseasesGLO1 protein, humanGlycation End Products, AdvancedLactoylglutathione LyasePyruvaldehydeCardiovascular diseaseDiabetes, cancerGlycationGlyoxalaseMethylglyoxalObesityRenal failureTherapeutics

Identifiers

PMID27406712
PMCPMC4975768
OpenAlexW2467090882

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.