Evidence map›Paper›PMID 24189185›Full record

ReviewSteroids2014

Role of aldo-keto reductase family 1 (AKR1) enzymes in human steroid metabolism.

Tea Lanišnik Rižner, Trevor M Penning

Abstract readReview
In one paragraph

Review in Steroids, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 103 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
103citing papers in PubMed, 1 pooled it
6.2field-weighted citation impact, top 3% 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

103 citing papers in PubMed, 1 synthesis or guideline pooled it, 209 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. AKR1B1 and AKR1B10 as Potential Prognostic Biomarkers of Endometrial Cancer.International journal of molecular sciences · 2026
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
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  14. Article
  15. Effect of Treatment on Steroidome in Women with Multiple Sclerosis.International journal of molecular sciences · 2025
    Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Altered Steroidome in Women with Multiple Sclerosis.International journal of molecular sciences · 2024
    Article

43 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

2 authors at 2 institutions in 2 countries.

Tea Lanišnik RižnerInstitute of Biochemistry, Faculty of Medicine, University of Ljubljana, Slovenia. Electronic address: tea.lanisnik-rizner@mf.uni-lj.si.
Trevor M PenningCenter of Excellence in Environmental Toxicology, Department of Pharmacology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA. Electronic address: penning@upenn.edu.
University of Ljubljana · SIUniversity of Pennsylvania · US

Funding

Translational Research Support CoreP30ES013508 · NIEHS · UNIVERSITY OF PENNSYLVANIA · PI Rebecca A Simmons · 2006 to 2026
$35.3M
Structure/Function of Steroid Transforming AKR'sR01DK047015 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI PENNING, TREVOR M · 1994 to 2011
$3.2M
Human Aldo Keto Reductases and Steroid Hormone ActionR01CA090744 · NCI · UNIVERSITY OF PENNSYLVANIA · PI PENNING, TREVOR M · 2001 to 2011
$3.1M
NCI NIH HHS 1R01-CA90744NCI NIH HHS R01 CA090744NIDDK NIH HHS 1R01-DK47015NIDDK NIH HHS R01 DK047015NIEHS NIH HHS P30 ES013508NIEHS NIH HHS P30-ES013508
6 · The paper itself

Abstract

Human aldo-keto reductases AKR1C1-AKR1C4 and AKR1D1 play essential roles in the metabolism of all steroid hormones, the biosynthesis of neurosteroids and bile acids, the metabolism of conjugated steroids, and synthetic therapeutic steroids. These enzymes catalyze NADPH dependent reductions at the C3, C5, C17 and C20 positions on the steroid nucleus and side-chain. AKR1C1-AKR1C4 act as 3-keto, 17-keto and 20-ketosteroid reductases to varying extents, while AKR1D1 acts as the sole Δ(4)-3-ketosteroid-5β-reductase (steroid 5β-reductase) in humans. AKR1 enzymes control the concentrations of active ligands for nuclear receptors and control their ligand occupancy and trans-activation, they also regulate the amount of neurosteroids that can modulate the activity of GABAA and NMDA receptors. As such they are involved in the pre-receptor regulation of nuclear and membrane bound receptors. Altered expression of individual AKR1C genes is related to development of prostate, breast, and endometrial cancer. Mutations in AKR1C1 and AKR1C4 are responsible for sexual development dysgenesis and mutations in AKR1D1 are causative in bile-acid deficiency.

Indexed as

20-Hydroxysteroid DehydrogenasesBile Acids and SaltsDisorders of Sex DevelopmentHumansMutationOxidoreductasesReceptors, Cytoplasmic and NuclearSteroids20-Hydroxysteroid Dehydrogenases3 alpha-beta, 20 beta-hydroxysteroid dehydrogenase3-oxo-5 beta-steroid delta 4-dehydrogenaseBile Acids and SaltsOxidoreductasesReceptors, Cytoplasmic and NuclearSteroidstrans-1,2-dihydrobenzene-1,2-diol dehydrogenase17β-hydroxysteroid dehydrogenase type 63α/β-Diol5α-androstane-3α/β,17β-diol5α-reductase type 1 or 25α/β-DHT5α/β-dihydrotestosteroneAKRaldo–keto reductaseandrogen receptorARBile-acidsCancerCARcastrate resistant prostate cancercatechol-O-methyl transferaseCOMTconstitutive androstane receptorCRPCCYPcytochrome P450 superfamilydisordered sexual dysgenesisDSDERestrogen receptorfarnesoid X receptorFXRGABAGPBAR1G protein coupled bile acid receptorHSD17B6Hydroxysteroid dehydrogenaseInherited mutationsMAFminor allelic frequencyNeurosteroidsNMDAN-methyl-d-aspartatePRpregnane X receptorprogesterone receptorPXRSDRshort-chain dehydrogenase/reductasesingle nucleotide differencesingle nucleotide polymorphismSNDSNPSRD5A1/A2sulfotransferaseSULTSynthetic steroidsUDP glucuronosyl transferaseUGTγ-aminobutyric acid

Identifiers

PMID24189185
PMCPMC3870468
OpenAlexW1978348589

What OpenQuestion holds

Textmetadata
LicenceTDM
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.