Evidence map›Paper›PMID 42909791›Full record

ReviewPharmacological reports : PR2026

Glycation stress in glioma: a metabolic vulnerability and therapeutic target.

Sonia B Umdor, Ellora Sen

Abstract readReview
PubMed Publisher
In one paragraph

Review in Pharmacological reports : PR, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

2 authors.

Sonia B UmdorNational Brain Research Centre, Manesar, Haryana, 122052, India.ORCID http://orcid.org/0000-0001-6172-0034
Ellora SenNational Brain Research Centre, Manesar, Haryana, 122052, India. ellora@nbrc.ac.in.ORCID http://orcid.org/0000-0001-6842-7850

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gliomas are primary brain tumors characterized by genetic heterogeneity, metabolic reprogramming, and resistance to therapy, which collectively contribute to tumor progression and aggressive clinical behavior. Heightened aerobic glycolysis in these tumors is associated with altered glycolytic flux and dysregulated metabolic landscape. The ubiquitous dicarbonyl metabolite methylglyoxal (MGO) is a highly reactive glycating agent produced from glycolytic intermediates. MGO is a major precursor of advanced glycation end products (AGEs), and excessive AGE accumulation is associated with disruption of cellular homeostasis. Inhibitors of key bioenergetic pathways have shown potential in glioma, indicating that altered glycolysis may create metabolic vulnerabilities that influence tumor cell survival. In this context, increased glycolytic flux in glioma may provide a mechanistic link between glycation stress and tumor progression. This review discusses the influence of glycation stress in glioma biology and emphasize the importance of considering genetic heterogeneity, redox landscape, and metabolic comorbidities to better understand glycation burden and inform therapeutic strategies.

Indexed as

AgeGliomaMetabolismMethylglyoxalNeuro-energetics

Identifiers

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.