Evidence map›Paper›PMID 33945128›Full record

ReviewAdvances in experimental medicine and biology2021

Aldo Keto Reductases AKR1B1 and AKR1B10 in Cancer: Molecular Mechanisms and Signaling Networks.

Sreeparna Banerjee

Abstract readReview
PubMed Publisher
In one paragraph

Review in Advances in experimental medicine and biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing 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

20 citing papers in PubMed.

  1. ExploringMolecules (Basel, Switzerland) · 2026
    Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Frontiers in molecular biosciences · 2025
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  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

1 author.

Sreeparna BanerjeeDepartment of Biological Sciences, Orta Dogu Teknik Universitesi (ODTU/METU), Ankara, Turkey. banerjee@metu.edu.tr.ORCID https://orcid.org/0000-0003-4596-6768

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Deregulation of metabolic pathways has increasingly been appreciated as a major driver of cancer in recent years. The principal cancer-associated alterations in metabolism include abnormal uptake of glucose and amino acids and the preferential use of metabolic pathways for the production of biomass and nicotinamide adenine dinucleotide phosphate (NADPH). Aldo-keto reductases (AKRs) are NADPH dependent cytosolic enzymes that can catalyze the reduction of carbonyl groups to primary and secondary alcohols using electrons from NADPH. Aldose reductase, also known as AKR1B1, catalyzes the conversion of excess glucose to sorbitol and has been studied extensively for its role in a number of diabetic pathologies. In recent years, however, high expression of the AKR1B and AKR1C family of enzymes has been strongly associated with worse outcomes in different cancer types. This review provides an overview of the catalysis-dependent and independent data emerging on the molecular mechanisms of the functions of AKRBs in different tumor models with an emphasis of the role of these enzymes in chemoresistance, inflammation, oxidative stress and epithelial-to-mesenchymal transition.

Indexed as

Aldehyde ReductaseAldo-Keto ReductasesNeoplasmsCatalysisDrug Resistance, NeoplasmEpithelial-Mesenchymal TransitionHumansInflammationNADPOxidative StressAKR1B10 protein, humanAKR1B1 protein, humanAldehyde ReductaseAldo-Keto ReductasesNADPAldo keto reductasesCancerChemoresistanceEpithelial-to-mesenchymal transitionInflammationOxidative stress

Identifiers

PMID33945128

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.