Evidence map›Paper›PMID 23297354›Full record

ReviewPhilosophical transactions of the Royal Society of London. Series B, Biological sciences2013

Human cytochromes P450 in health and disease.

Daniel W Nebert, Kjell Wikvall, Walter L Miller

Open access · bronzeAbstract readReview
In one paragraph

Review in Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 213 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
213citing papers in PubMed, 1 pooled it
40.5field-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

213 citing papers in PubMed, 1 synthesis or guideline pooled it, 500 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. The Impact of Genetic Factors in Ménière's Disease.International journal of molecular sciences · 2026
    Review
  6. Preliminary Study on Sexual Maturation Pattern ofInternational journal of molecular sciences · 2026
    Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. Review
  17. Caenorhabditis Elegans as a Model for Environmental Epigenetics.Current environmental health reports · 2025
    Review
  18. Review
  19. Article
  20. Review

153 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 3 institutions in 2 countries.

Daniel W NebertDepartment of Environmental Health, Center for Environmental Genetics, University of Cincinnati Medical Center, Cincinnati, OH 45267-0056, USA. dan.nebert@uc.edu
Kjell Wikvall
Walter L Miller
University of California, San Francisco · USUniversity of Cincinnati · USUppsala University · SE

Funding

REPRODUCTIVE AND DEVELOPMENTAL TOXICOLOGY RESEARCHP30ES006096 · NIEHS · UNIVERSITY OF CINCINNATI · PI YADAV, JAGJIT S · 1992 to 2022
$35.4M
Molecular Biology of Steroidogenic ProteinsR01DK037922 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI MILLER, WALTER L. · 1987 to 2011
$2.8M
NIDDK NIH HHS R01 DK037922NIEHS NIH HHS P30 ES006096NIGMS NIH HHS R01 GM037020
6 · The paper itself

Abstract

There are 18 mammalian cytochrome P450 (CYP) families, which encode 57 genes in the human genome. CYP2, CYP3 and CYP4 families contain far more genes than the other 15 families; these three families are also the ones that are dramatically larger in rodent genomes. Most (if not all) genes in the CYP1, CYP2, CYP3 and CYP4 families encode enzymes involved in eicosanoid metabolism and are inducible by various environmental stimuli (i.e. diet, chemical inducers, drugs, pheromones, etc.), whereas the other 14 gene families often have only a single member, and are rarely if ever inducible or redundant. Although the CYP2 and CYP3 families can be regarded as largely redundant and promiscuous, mutations or other defects in one or more genes of the remaining 16 gene families are primarily the ones responsible for P450-specific diseases-confirming these genes are not superfluous or promiscuous but rather are more directly involved in critical life functions. P450-mediated diseases comprise those caused by: aberrant steroidogenesis; defects in fatty acid, cholesterol and bile acid pathways; vitamin D dysregulation and retinoid (as well as putative eicosanoid) dysregulation during fertilization, implantation, embryogenesis, foetogenesis and neonatal development.

Indexed as

AnimalsCholesterolCytochrome P-450 Enzyme SystemDehydroepiandrosteroneEicosanoidsEnzyme ActivationEvolution, MolecularHumansHydroxylationMetabolic DiseasesMultigene FamilyOxidation-ReductionPregnenoloneTretinoinVitamin DCholesterolCytochrome P-450 Enzyme SystemDehydroepiandrosteroneEicosanoidsPregnenoloneTretinoinVitamin D

Identifiers

PMID23297354
PMCPMC3538421
OpenAlexW2147971048

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.