Evidence map›Paper›PMID 22415012›Full record

ArticleMolecular medicine (Cambridge, Mass.)2012

A CYP26B1 polymorphism enhances retinoic acid catabolism and may aggravate atherosclerosis.

Olesya Krivospitskaya, Ali Ateia Elmabsout, Eva Sundman, Leif A Söderström, Olga Ovchinnikova, Andreas C Gidlöf, Nikolai Scherbak, Giuseppe Danilo Norata, Ann Samnegård, Hans Törmä and 5 more

Open access · goldAbstract read
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
0.8field-weighted citation impact, top 30% 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

23 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Retinoic acid signaling and metabolism in heart failure.American journal of physiology. Heart and circulatory physiology · 2025
    Review
  3. Review
  4. Review
  5. Immunometabolic effects ofImmunometabolism (Cobham, Surrey) · 2024
    Review
  6. Article
  7. β-carotene accelerates the resolution of atherosclerosis in mice.bioRxiv : the preprint server for biology · 2024
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Inhibition of theDrug metabolism and disposition: the biological fate of chemicals · 2017
    Article
  17. Review
  18. Article
  19. Article
  20. Review
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

15 authors at 5 institutions in 3 countries.

Olesya KrivospitskayaDepartment of Clinical Medicine, School of Health and Medical Sciences, Örebro University, Örebro, Sweden.
Ali Ateia Elmabsout
Eva Sundman
Leif A Söderström
Olga Ovchinnikova
Andreas C Gidlöf
Nikolai Scherbak
Giuseppe Danilo Norata
Ann Samnegård
Hans Törmä
Samy M Abdel-Halim
Jan-Håkan Jansson
Per Eriksson
Allan Sirsjö
Peder S Olofsson
Karolinska Institutet · SEÖrebro University · SEKarolinska University Hospital · SESkellefteå Hospital · SEUppsala University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

All-trans retinoic acid, controlled by cytochrome P450, family 26 (CYP26) enzymes, potentially has beneficial effects in atherosclerosis treatment. This study investigates CYP26 subfamily B, polypeptide 1 (CYP26B1) in atherosclerosis and the effects of a genetic polymorphism in CYP26B1 on retinoid catabolism. We found that CYP26B1 mRNA was induced by retinoic acid in human atherosclerotic arteries, and CYP26B1 and the macrophage marker CD68 were colocalized in human atherosclerotic lesions. In mice, Cyp26B1 mRNA was higher in atherosclerotic arteries than in normal arteries. Databases were queried for nonsynonymous CYP26B1 single nucleotide polymorphisms (SNPs) and rs2241057 selected for further studies. Constructs of the CYP26B1 variants were created and used for production of purified proteins and transfection of macrophagelike cells. The minor variant catabolized retinoic acid with significantly higher efficiency, indicating that rs2241057 is functional and suggesting reduced retinoid availability in tissues with the minor variant. rs2241057 was investigated in a Stockholm Coronary Atherosclerosis Risk Factor (SCARF) subgroup. The minor allele was associated with slightly larger lesions, as determined by angiography. In summary, this study identifies the first CYP26B1 polymorphism that alters CYP26B1 capacity to metabolize retinoic acid. CYP26B1 was expressed in macrophage-rich areas of human atherosclerotic lesions, induced by retinoic acid and increased in murine atherosclerosis. Taken together, the results indicate that CYP26B1 capacity is genetically regulated and suggest that local CYP26B1 activity may influence atherosclerosis.

Indexed as

Polymorphism, Single NucleotideAllelesAnimalsAtherosclerosisCell LineCytochrome P-450 Enzyme SystemFemaleGene ExpressionGenotypeHumansMacrophagesMiceMice, Inbred C57BLMice, KnockoutMiddle AgedProtein TransportCytochrome P-450 Enzyme SystemRetinoic Acid 4-HydroxylaseRNA, MessengerTretinoin

Identifiers

PMID22415012
PMCPMC3388133
OpenAlexW1546576396

What OpenQuestion holds

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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.