Evidence map›Paper›PMID 33925454›Full record

ReviewInternational journal of molecular sciences2021

The Role of Leptin in Fetal Growth during Pre-Eclampsia.

Victoria E de Knegt, Paula L Hedley, Jørgen K Kanters, Ida N Thagaard, Lone Krebs, Michael Christiansen, Ulrik Lausten-Thomsen

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 2 pooled it
7.1field-weighted citation impact, top 2% 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

31 citing papers in PubMed, 2 syntheses or guidelines pooled it, 51 citations in OpenAlex.

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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

7 authors at 5 institutions in 1 country.

Victoria E de KnegtDepartment for Congenital Disorders, Danish National Biobank and Biomarkers, Statens Serum Institute, Artillerivej 5, 2300 Copenhagen, Denmark.
Paula L HedleyDepartment for Congenital Disorders, Danish National Biobank and Biomarkers, Statens Serum Institute, Artillerivej 5, 2300 Copenhagen, Denmark.ORCID 0000-0001-5801-960X
Jørgen K KantersLaboratory of Experimental Cardiology, Department of Biomedical Science, University of Copenhagen, Blegdamsvej 3B, 2200 Copenhagen, Denmark.ORCID 0000-0002-3267-4910
Ida N ThagaardDepartment of Gynecology and Obstetrics, Copenhagen University Hospital Slagelse, Ingemannsvej 18, 4200 Slagelse, Denmark.
Lone KrebsDepartment of Obstetrics and Gynecology, University Hospital Hvidovre, Kettegård Alle 30, 2650 Hvidovre, Denmark.ORCID 0000-0001-5433-4776
Michael ChristiansenDepartment for Congenital Disorders, Danish National Biobank and Biomarkers, Statens Serum Institute, Artillerivej 5, 2300 Copenhagen, Denmark.ORCID 0000-0003-4713-755X
Ulrik Lausten-ThomsenDepartment of Neonatology, University Hospital Rigshospitalet, Blegdamsvej 9, 2100 Copenhagen, Denmark.
Statens Serum Institut · DKCopenhagen University Hospital · DKHvidovre Hospital · DKRigshospitalet · DKUniversity of Copenhagen · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Leptin is secreted by the placenta and has a multi-facetted role in the regulation of functions related to pregnancy. Metabolic disorders and insufficient homeostatic compensatory mechanisms involving leptin during pregnancy play a decisive role in the development of pre-eclampsia (PE) and give rise to compromised intrauterine growth conditions and aberrant birth weight of offspring. This review was compiled to elucidate the metabolic background of PE and its relationship with adverse intrauterine growth conditions through the examination of leptin as well as to describe possible mechanisms linking leptin to fetal growth restriction. This review illustrates that leptin in PE is dysregulated in maternal, fetal, and placental compartments. There is no single set of unifying mechanisms within the spectrum of PE, and regulatory mechanisms involving leptin are specific to each situation. We conclude that dysregulated leptin is involved in fetal growth at many levels through complex interactions with parallel pregnancy systems and probably throughout the entirety of pregnancy.

Indexed as

AnimalsFemaleFetal Growth RetardationHumansLeptinPlacentaPre-EclampsiaPregnancyReceptors, LeptinLEP protein, humanLeptinReceptors, Leptinanthropometrybirth weightfetal developmentfetal growth restrictioninfant growthleptinpre-eclampsiaprenatal growth

Identifiers

PMID33925454
PMCPMC8123779
OpenAlexW3158131352

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.