Evidence map›Paper›PMID 25802092›Full record

ReviewMolecular immunology2015

The complement system and adverse pregnancy outcomes.

Jean F Regal, Jeffrey S Gilbert, Richard M Burwick

Open access · greenAbstract readReview
In one paragraph

Review in Molecular immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
91citing papers in PubMed, 2 pooled it
11.4field-weighted citation impact, top 1% 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

91 citing papers in PubMed, 2 syntheses or guidelines pooled it, 166 citations in OpenAlex.

  1. Pooled it
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  16. Sialidases derived frombioRxiv : the preprint server for biology · 2025
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31 more citing papers are in PubMed but not listed here.

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

3 authors at 2 institutions in 1 country.

Jean F RegalDepartment of Biomedical Sciences, University of Minnesota Medical School, 1035 University Drive, Duluth, MN 55812, USA. Electronic address: jregal@d.umn.edu.
Jeffrey S GilbertDepartment of Biomedical Sciences, University of Minnesota Medical School, 1035 University Drive, Duluth, MN 55812, USA. Electronic address: jgilbert@d.umn.edu.
Richard M BurwickDepartment of Obstetrics and Gynecology, Division of Maternal Fetal Medicine, Oregon Health & Science University, Mail Code: L-458, 3181 SW Sam Jackson Park Road, Portland, OR 97239, USA. Electronic address: burwick@ohsu.edu.
University of Minnesota, Duluth · USOregon Health & Science University · US

Funding

Complement Activation in Pregnancy and HypertensionR15HL109843 · NHLBI · UNIVERSITY OF MINNESOTA DULUTH · PI REGAL, JEAN F. · 2011 to 2015
$1.3M
In vivo probes for the APJ receptor.R01HD079547 · NICHD · RESEARCH TRIANGLE INSTITUTE · PI MAITRA, RANGAN, RUNYON, SCOTT P · 2014 to 2016
$1.3M
NHLBI NIH HHS R15 HL109843NHLBI NIH HHS R15HL109843NICHD NIH HHS R01 HD079547NICHD NIH HHS R01HD079547-01
6 · The paper itself

Abstract

Adverse pregnancy outcomes significantly contribute to morbidity and mortality for mother and child, with lifelong health consequences for both. The innate and adaptive immune system must be regulated to insure survival of the fetal allograft, and the complement system is no exception. An intact complement system optimizes placental development and function and is essential to maintain host defense and fetal survival. Complement regulation is apparent at the placental interface from early pregnancy with some degree of complement activation occurring normally throughout gestation. However, a number of pregnancy complications including early pregnancy loss, fetal growth restriction, hypertensive disorders of pregnancy and preterm birth are associated with excessive or misdirected complement activation, and are more frequent in women with inherited or acquired complement system disorders or complement gene mutations. Clinical studies employing complement biomarkers in plasma and urine implicate dysregulated complement activation in components of each of the adverse pregnancy outcomes. In addition, mechanistic studies in rat and mouse models of adverse pregnancy outcomes address the complement pathways or activation products of importance and allow critical analysis of the pathophysiology. Targeted complement therapeutics are already in use to control adverse pregnancy outcomes in select situations. A clearer understanding of the role of the complement system in both normal pregnancy and complicated or failed pregnancy will allow a rational approach to future therapeutic strategies for manipulating complement with the goal of mitigating adverse pregnancy outcomes, preserving host defense, and improving long term outcomes for both mother and child.

Indexed as

StillbirthAnimalsComplement ActivationComplement System ProteinsFemaleFetal Growth RetardationFetusGene ExpressionHumansHypertension, Pregnancy-InducedMiceMutationPlacentaPregnancyPremature BirthRatsComplement System ProteinsComplement systemFetal growth restrictionMiscarriagePlacentaPreeclampsiaPregnancyPreterm birth

Identifiers

PMID25802092
PMCPMC4447554
OpenAlexW1971154967

What OpenQuestion holds

Textmetadata
LicenceTDM
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.