Evidence map›Paper›PMID 25710174›Full record

ArticlePloS one2015

Genetic analysis of membrane cofactor protein (CD46) of the complement system in women with and without preeclamptic pregnancies.

A Inkeri Lokki, Tia Aalto-Viljakainen, Seppo Meri, Hannele Laivuori, FINNPEC

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 14% 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

12 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.

  1. Pooled it
  2. Observational
  3. Review
  4. Review
  5. Review
  6. Article
  7. Genetics of recurrent pregnancy loss among Iranian population.Molecular genetics & genomic medicine · 2019
    Review
  8. The role of the complement system in HIV infection and preeclampsia.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2019
    Review
  9. The Immunogenetic Conundrum of Preeclampsia.Frontiers in immunology · 2018
    Review
  10. Complement activation, a threat to pregnancy.Seminars in immunopathology · 2018
    Review
  11. Article
  12. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

A Inkeri LokkiDepartment of Medical Genetics, Haartman Institute, University of Helsinki, Helsinki, Finland; Department of Bacteriology and Immunology, Haartman Institute, University of Helsinki, Helsinki, Finland; Immunobiology research program, Research Programs Unit, University of Helsinki, Helsinki, Finland.
Tia Aalto-ViljakainenDepartment of Medical Genetics, Haartman Institute, University of Helsinki, Helsinki, Finland; Department of Obstetrics and Gynecology, University of Helsinki and Helsinki University Central Hospital, Helsinki, Finland.
Seppo MeriDepartment of Bacteriology and Immunology, Haartman Institute, University of Helsinki, Helsinki, Finland; Immunobiology research program, Research Programs Unit, University of Helsinki, Helsinki, Finland.
Hannele LaivuoriDepartment of Medical Genetics, Haartman Institute, University of Helsinki, Helsinki, Finland; Department of Obstetrics and Gynecology, University of Helsinki and Helsinki University Central Hospital, Helsinki, Finland; Finnish Institute for Molecular Medicine, University of Helsinki, Helsinki, Finland.
FINNPEC
University of Helsinki · FI

Funding

Wellcome Trust
6 · The paper itself

Abstract

Preeclampsia is a common disorder of pregnancy characterized by endothelial dysfunction. It may be life-threatening for the mother and fetus in severe cases. Dysregulation of the complement system has been suggested to predispose women to preeclampsia. Complement is part of the innate and adaptive immune systems and potentially capable of causing inflammation and tissue damage. Membrane cofactor protein MCP (CD46) is among the potent complement regulators that have recently been linked to a severe form of preeclampsia with or without an underlying autoimmune phenotype. Mutations in CD46 predispose to thrombotic microangiopathy with endothelial cell dysfunction. The exome of CD46 were sequenced in 95 Finnish women with severe preeclampsia. Genetic variations discovered in the full exome were compared to those observed in 95 control women who did not develop preeclampsia. Because A304V (rs35366573) was associated with preeclampsia in one previous study, we sequenced the transmembrane region including the A304V variant and part of the cytoplasmic tail in 95 additional controls. We did not discover any association between A304V or other CD46 SNPs and preeclampsia. This study describes a carefully characterized cohort of severely preeclamptic Finnish women and found no potentially predisposing variants in CD46. However, it is possible that other genetic components of the complement system may affect the pathogenesis of severe preeclampsia and related diseases.

Indexed as

AdultCohort StudiesComplement System ProteinsExomeExonsFemaleGenetic TestingGenotypeHumansMembrane Cofactor ProteinOdds RatioPolymorphism, Single NucleotidePre-EclampsiaPregnancySequence Analysis, DNASeverity of Illness IndexComplement System ProteinsMembrane Cofactor Protein

Identifiers

PMID25710174
PMCPMC4339547
OpenAlexW2081092344

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.