Evidence map›Paper›PMID 27842594›Full record

ArticleLipids in health and disease2016

Fetal gender and gestational age differentially affect PCSK9 levels in intrauterine growth restriction.

Ulrich Pecks, Werner Rath, Nicolai Maass, Bartlomiej Berger, Imke Lueg, André Farrokh, Sabrina Farrokh, Christel Eckmann-Scholz

Open access · goldAbstract read
In one paragraph

Article in Lipids in health and disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

17 citing papers in PubMed, 31 citations in OpenAlex.

  1. The physiological effects of APOE genotype in healthy young/middle-aged individuals.Biological reviews of the Cambridge Philosophical Society · 2026
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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

8 authors at 3 institutions in 1 country.

Ulrich PecksDepartment of Obstetrics and Gynecology, University Hospital of the RWTH, Aachen, Germany. Ulrich.Pecks@uksh.de.
Werner RathDepartment of Obstetrics and Gynecology, University Hospital Schleswig-Holstein, Kiel, Germany.
Nicolai MaassDepartment of Obstetrics and Gynecology, University Hospital Schleswig-Holstein, Kiel, Germany.
Bartlomiej BergerDepartment of Obstetrics and Gynecology, University Hospital of the RWTH, Aachen, Germany.
Imke LuegDepartment of Obstetrics and Gynecology, University Hospital of the RWTH, Aachen, Germany.
André FarrokhDepartment of Obstetrics and Gynecology, University Hospital Schleswig-Holstein, Kiel, Germany.
Sabrina FarrokhDepartment of Obstetrics and Gynecology, University Hospital Schleswig-Holstein, Kiel, Germany.
Christel Eckmann-ScholzDepartment of Obstetrics and Gynecology, University Hospital Schleswig-Holstein, Kiel, Germany.
RWTH Aachen University · DEUniversity of Lübeck · DEUniversity Hospital Schleswig-Holstein · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMaternal and fetal Low Density Lipoprotein-Cholesterol (LDL-C) concentrations are compromised in intrauterine growth restriction (IUGR). Generally, LDL-C catabolism is under control of PCSK9 by binding to the LDL-receptor leading to its degradation. Hence, we hypothesized a role for PCSK9 in the modulation of lipid metabolism and placental transport in IUGR.

methods172 women, 70 IUGR and 102 controls were included in the study. Maternal and fetal serum PCSK9 levels and lipid profiles including LDL-C were measured. Placental LDL-receptor and PCSK9 expressions were estimated by tissue microarray immunohistochemistry, and analyzed by two blinded observers using an immunoreactivity score. Non-parametric tests and multivariate regression analyses were used for statistical estimations.

resultsPCSK9 levels in the maternal and fetal compartment independently predicted LDL-C levels (maternal compartment: adjusted R

conclusionsOur results suggest that PCSK9 play a role in impaired fetal growth by controlling fetal LDL-C metabolism, which seems to be dependent on gestational age and fetal gender. This underlines the need to identify subgroups of IUGR that may benefit from individualized and gender-specific pharmacotherapy in future studies.

Indexed as

Gene Expression Regulation, DevelopmentalGestational AgeAdultFemaleFetal Growth RetardationHumansMalePregnancyProprotein Convertase 9Receptors, LDLSex FactorsLDLR protein, humanPCSK9 protein, humanProprotein Convertase 9Receptors, LDLcholesterol metabolismIntrauterine growth restriction (IUGR)LDL-CLDL receptorPCSK9

Identifiers

PMID27842594
PMCPMC5109703
OpenAlexW2556118492

What OpenQuestion holds

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Registered trials

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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.