Evidence map›Paper›PMID 25264875›Full record

ReviewPloS one2014

Pathway analysis of genetic factors associated with spontaneous preterm birth and pre-labor preterm rupture of membranes.

Antonio Capece, Olga Vasieva, Shireen Meher, Zarko Alfirevic, Ana Alfirevic

Open access · goldAbstract readReview
In one paragraph

Review in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
5.4field-weighted citation impact, top 4% 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

46 citing papers in PubMed, 79 citations in OpenAlex.

  1. Article
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  12. Genetics, epigenetics, and transcriptomics of preterm birth.American journal of reproductive immunology (New York, N.Y. : 1989) · 2022
    Review
  13. IL-27 Mediates Th1 Cells Infiltration in Fetal Membranes in Preterm Labor.Reproductive sciences (Thousand Oaks, Calif.) · 2022
    Article
  14. Article
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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

5 authors at 1 institution in 1 country.

Antonio CapeceDepartment of Women's and Children's Health, Institute of Translational Medicine, University of Liverpool, Liverpool, United Kingdom.
Olga VasievaInstitute of Integrative Biology, University of Liverpool, Liverpool, United Kingdom.
Shireen MeherDepartment of Women's and Children's Health, Institute of Translational Medicine, University of Liverpool, Liverpool, United Kingdom.
Zarko AlfirevicDepartment of Women's and Children's Health, Institute of Translational Medicine, University of Liverpool, Liverpool, United Kingdom.
Ana AlfirevicDepartment of Molecular and Clinical Pharmacology, Institute of Translational Medicine, University of Liverpool, Liverpool, United Kingdom.
University of Liverpool · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPre-term birth (PTB) remains the leading cause of infant mortality and morbidity. Its etiology is multifactorial, with a strong genetic component. Genetic predisposition for the two subtypes, spontaneous PTB with intact membranes (sPTB) and preterm prelabor rapture of membranes (PPROM), and differences between them, have not yet been systematically summarised. METHODS AND

findingsOur literature search identified 15 association studies conducted in 3,600 women on 2175 SNPs in 274 genes. We used Ingenuity software to impute gene pathways and networks related to sPTB and PPROM. Detailed insight in the defined functional ontologies clearly separated integrated datasets for sPTB and PPROM. Our analysis of upstream regulators of genes suggests that glucocorticoid receptor (NR3C1), peroxisome proliferator activated receptor γ (PPARG) and interferon regulating factor 3 (IRF3) may be sPTB specific. PPROM-specific genes may be regulated by estrogen receptor2 (ESR2) and signal transducer and activator of transcription (STAT1). The inflammatory transcription factor NFκB is linked to both sPTB and PPROM, however, their inflammatory response is distinctly different.

conclusionsBased on our analyses, we propose an autoimmune/hormonal regulation axis for sPTB, whilst pathways implicated in the etiology of PPROM include hematologic/coagulation function disorder, collagen metabolism, matrix degradation and local inflammation. Our hypothesis generating study has identified new candidate genes in the pathogenesis of PPROM and sPTB, which should be validated in large cohorts.

Indexed as

AutoimmunityFemaleGenetic Predisposition to DiseaseHumansInfantInfant MortalityInfant, NewbornInterferon Regulatory Factor-3NF-kappa BPolymorphism, GeneticPPAR gammaPregnancyPregnancy ComplicationsPremature BirthPremature Rupture of Fetal MembranesReceptors, EstrogenInterferon Regulatory Factor-3IRF3 protein, humanNF-kappa BNR3C1 protein, humanPPAR gammaReceptors, EstrogenReceptors, GlucocorticoidSTAT1 protein, humanSTAT1 Transcription Factor

Identifiers

PMID25264875
PMCPMC4181300
OpenAlexW2169278993

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.