Evidence map›Paper›PMID 32472014›Full record

ArticleScientific reports2020

CYP17A1 deficient XY mice display susceptibility to atherosclerosis, altered lipidomic profile and atypical sex development.

Redouane Aherrahrou, Alexandra E Kulle, Natalia Alenina, Ralf Werner, Simeon Vens-Cappell, Michael Bader, Heribert Schunkert, Jeanette Erdmann, Zouhair Aherrahrou

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

28 citing papers in PubMed, 44 citations in OpenAlex.

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  10. Regulation of early gonocyte differentiation in zebrafish.Biochemical Society transactions · 2025
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  17. Androgen signaling inhibitsZoological research · 2024
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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

9 authors at 6 institutions in 2 countries.

Redouane AherrahrouInstitute for Cardiogenetics, University of Lübeck, Lübeck, Germany.
Alexandra E KulleDepartment of Pediatrics, Division of Pediatric Endocrinology and Diabetes, University Hospital Schleswig-Holstein, Christian-Albrechts-University, Kiel, Germany.
Natalia AleninaMax-Delbrück-Center for Molecular Medicine (MDC), Robert-Rössle-Str. 10, 13125, Berlin, Germany.ORCID http://orcid.org/0000-0002-6071-5433
Ralf WernerDepartment of Pediatrics, Division of Pediatric Endocrinology and Diabetes, University of Lübeck, Lübeck, Germany.ORCID http://orcid.org/0000-0003-3718-3595
Simeon Vens-CappellBioanalytical Core Facility, CBBM (Center of Brain Behavior and Metabolism), University of Lübeck, Lübeck, Germany.ORCID http://orcid.org/0000-0003-4773-4653
Michael BaderMax-Delbrück-Center for Molecular Medicine (MDC), Robert-Rössle-Str. 10, 13125, Berlin, Germany.
Heribert SchunkertKardiologie, Deutsches Herzzentrum München, Technische Universität München and DZHK (German Centre for Cardiovascular Research), Partner Site Munich Heart Alliance, Munich, Germany.
Jeanette Erdmann *Institute for Cardiogenetics, University of Lübeck, Lübeck, Germany.ORCID http://orcid.org/0000-0002-4486-6231
Zouhair Aherrahrou *Institute for Cardiogenetics, University of Lübeck, Lübeck, Germany. zouhair.aherrahrou@uni-luebeck.de.
Max Delbrück Center · DEUniversität Hamburg · DEUniversity of Lübeck · DEChristian-Albrechts-Universität zu Kiel · DEGerman Centre for Cardiovascular Research · DEUniversity of Virginia · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

CYP17A1 is a cytochrome P450 enzyme with 17-alpha-hydroxylase and C17,20-lyase activities. CYP17A1 genetic variants are associated with coronary artery disease, myocardial infarction and visceral and subcutaneous fat distribution; however, the underlying pathological mechanisms remain unknown. We aimed to investigate the function of CYP17A1 and its impact on atherosclerosis in mice. At 4-6 months, CYP17A1-deficient mice were viable, with a KO:Het:WT ratio approximating the expected Mendelian ratio of 1:2:1. All Cyp17a1 knockout (KO) mice were phenotypically female; however, 58% were Y chromosome-positive, resembling the phenotype of human CYP17A1 deficiency, leading to 46,XY differences/disorders of sex development (DSD). Both male and female homozygous KO mice were infertile, due to abnormal genital organs. Plasma steroid analyses revealed a complete lack of testosterone in XY-KO mice and marked accumulation of progesterone in XX-KO mice. Elevated corticosterone levels were observed in both XY and XX KO mice. In addition, Cyp17a1 heterozygous mice were also backcrossed onto an Apoe KO atherogenic background and fed a western-type diet (WTD) to study the effects of CYP17A1 on atherosclerosis. Cyp17a1 x Apoe double KO XY mice developed more atherosclerotic lesions than Apoe KO male controls, regardless of diet (standard or WTD). Increased atherosclerosis in CYP17A1 XY KO mice lacking testosterone was associated with altered lipid profiles. In mice, CYP17A1 deficiency interferes with sex differentiation. Our data also demonstrate its key role in lipidomic profile, and as a risk factor in the pathogenesis of atherosclerosis.

Indexed as

AnimalsAtherosclerosisChromatography, LiquidDiet, WesternDisease Models, AnimalFemaleInfertilityLipidomicsMaleMass SpectrometryMiceMice, KnockoutPhenotypeSteroid 17-alpha-HydroxylaseSteroidsSteroid 17-alpha-HydroxylaseSteroids

Identifiers

PMID32472014
PMCPMC7260244
OpenAlexW3031585628

What OpenQuestion holds

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LicenceCC BY
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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.