Evidence map›Paper›PMID 29580923›Full record

ArticlePregnancy hypertension2018

Endoglin pathway genetic variation in preeclampsia: A validation study in Norwegian and Latina cohorts.

Mandy J Schmella, James M Roberts, Yvette P Conley, Dianxu Ren, Gro L Storvold, Sue A Ingles, Melissa L Wilson, Anne Catherine Staff, Carl A Hubel

Open access · hybridAbstract readMulticenter StudyValidation Study
In one paragraph

Article in Pregnancy hypertension, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
2.4field-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

6 citing papers in PubMed, 18 citations in OpenAlex.

  1. VASCULAR AND RENAL MECHANISMS OF PREECLAMPSIA.Current opinion in physiology · 2023
    Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
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 4 institutions in 2 countries.

Mandy J SchmellaDepartment of Health Promotion and Development (School of Nursing), University of Pittsburgh, Pittsburgh, PA, USA. Electronic address: mjb111@pitt.edu.
James M RobertsDepartment of Obstetrics, Gynecology, & Reproductive Sciences (School of Medicine), University of Pittsburgh, PA, USA; Magee-Womens Research Institute, Pittsburgh, PA, USA; Department of Epidemiology (Graduate School of Public Health), University of Pittsburgh, Pittsburgh, PA, USA; Clinical and Translational Science Institute, University of Pittsburgh, Pittsburgh, PA, USA; Global Pregnancy Collaboration, USA. Electronic address: jroberts@mwri.magee.edu.
Yvette P ConleyDepartment of Health Promotion and Development (School of Nursing), University of Pittsburgh, Pittsburgh, PA, USA; Department of Human Genetics (Graduate School of Public Health), University of Pittsburgh, Pittsburgh, PA, USA. Electronic address: yconley@pitt.edu.
Dianxu RenDepartment of Health and Community Systems (School of Nursing), University of Pittsburgh, Pittsburgh, PA, USA. Electronic address: dir8@pitt.edu.
Gro L StorvoldFaculty of Medicine, University of Oslo, Oslo, Norway; Division of Obstetrics and Gynaecology, Oslo University Hospital, Oslo, Norway. Electronic address: g.l.storvold@medisin.uio.no.
Sue A InglesDepartment of Obstetrics and Gynecology (Keck School of Medicine), University of Southern California, Los Angeles, CA, USA; Department of Preventive Medicine (Keck School of Medicine), University of Southern California, Los Angeles, CA, USA. Electronic address: ingles@usc.edu.
Melissa L WilsonDepartment of Preventive Medicine (Keck School of Medicine), University of Southern California, Los Angeles, CA, USA; Global Pregnancy Collaboration, USA. Electronic address: melisslw@usc.edu.
Anne Catherine StaffFaculty of Medicine, University of Oslo, Oslo, Norway; Division of Obstetrics and Gynaecology, Oslo University Hospital, Oslo, Norway; Global Pregnancy Collaboration, USA. Electronic address: a.c.staff@medisin.uio.no.
Carl A HubelDepartment of Obstetrics, Gynecology, & Reproductive Sciences (School of Medicine), University of Pittsburgh, PA, USA; Magee-Womens Research Institute, Pittsburgh, PA, USA; Department of Environmental and Occupational Health (Graduate School of Public Health), University of Pittsburgh, Pittsburgh, PA, USA. Electronic address: chubel@mwri.magee.edu.
University of Pittsburgh · USUniversity of Oslo · NOUniversity of Southern California · USMagee-Womens Research Institute · US

Funding

Targeting Research and Academic Training of Nurses in GenomicsT32NR009759 · NINR · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI CONLEY, YVETTE P · 2006 to 2025
$4.5M
Mechanisms Modulating the Association between the ENG Pathway and PreeclampsiaF32NR014622 · NINR · MAGEE-WOMEN'S RES INST AND FOUNDATION · PI SCHMELLA, MANDY JO · 2013 to 2014
$97k
NINR NIH HHS F32 NR014622NINR NIH HHS T32 NR009759
6 · The paper itself

Abstract

objectiveThe purpose of this study was to validate our previous genetic association findings related to the endoglin (ENG) pathway from an American Caucasian preeclampsia cohort in independent preeclampsia cohorts. We also sought to explore the ENG pathway for new genetic associations in these independent cohorts. STUDY

designWe used a tagging single nucleotide (tSNP) approach to assess genetic variability across five ENG pathway genes (ENG, TGFβ1, TGFβR1, ALK1, and TGFβR2) in a Caucasian cohort from Norway (n = 77 preeclampsia cases & n = 63 normotensive controls) and a White Hispanic cohort from Southern California (n = 69 preeclampsia cases & n = 106 normotensive controls).

main outcome measuresUnivariate analyses (Chi Square, Fisher's Exact) and multivariate logistic regression were conducted to evaluate the association between tSNP genotype distributions and pregnancy outcome in each cohort. Logistic regression models were adjusted for maternal age at delivery, infant sex, parity, smoking during pregnancy, and pre-pregnancy BMI.

resultsAlthough we were unable to replicate our previous SNP-specific findings (ENG rs11792480, rs10121110; TGFβR2 rs6550005; p's > 0.05), we found that genetic variation in TGFβR1[ALK5] (rs6478974) and TGFβR2 (rs11129420, rs6802220, rs1155708, rs3773640, rs3773663) was significantly associated with preeclampsia in the Norwegian cohort and genetic variation in ALK1 (rs706819) and TGFβR2 (rs9843942) was significantly associated with preeclampsia in the Latina cohort.

conclusionOverall, our results provide further support for the involvement and investigation of the endoglin pathway in preeclampsia.

Indexed as

Polymorphism, Single NucleotideActivin Receptors, Type IIAdolescentAdultCaliforniaCase-Control StudiesChi-Square DistributionEndoglinFemaleGenetic Association StudiesGenetic Predisposition to DiseaseHispanic or LatinoHumansLogistic ModelsMultivariate AnalysisNorwayActivin Receptors, Type IIACVRL1 protein, humanEndoglinENG protein, humanProtein Serine-Threonine KinasesReceptors, Transforming Growth Factor betaReceptor, Transforming Growth Factor-beta Type IReceptor, Transforming Growth Factor-beta Type IITGFB1 protein, humanTGFBR1 protein, humanTransforming Growth Factor beta1Candidate geneEndoglinGenetic associationPreeclampsiaPregnancy

Identifiers

PMID29580923
PMCPMC5995147
OpenAlexW2770288056

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.