Evidence map›Paper›PMID 29366364›Full record

ArticleJournal of the renin-angiotensin-aldosterone system : JRAAS

Contribution of angiotensinogen M235T and T174M gene variants and haplotypes to preeclampsia and its severity in (North African) Tunisians.

Hedia Zitouni, Marwa Ben Ali Gannoum, Nozha Raguema, Wided Maleh, Ines Zouari, Raja El Faleh, Jean Guibourdenche, Wassim Y Almawi, Touhami Mahjoub

Open access · hybridAbstract read
In one paragraph

Article in Journal of the renin-angiotensin-aldosterone system : JRAAS. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 13% 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

4 citing papers in PubMed, 1 synthesis or guideline pooled it, 18 citations in OpenAlex.

  1. Three polymorphisms of renin-angiotensin system and preeclampsia risk.Journal of assisted reproduction and genetics · 2020
    Pooled it
  2. Review
  3. T174M-M235TCurrent issues in molecular biology · 2026
    Article
  4. Review
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.

Hedia Zitouni1 Laboratory of Human Genome and Multifactorial Diseases (LR12ES07), College of Pharmacy, University of Monastir, Tunisia.
Marwa Ben Ali Gannoum1 Laboratory of Human Genome and Multifactorial Diseases (LR12ES07), College of Pharmacy, University of Monastir, Tunisia.
Nozha Raguema1 Laboratory of Human Genome and Multifactorial Diseases (LR12ES07), College of Pharmacy, University of Monastir, Tunisia.
Wided Maleh4 Centre of Maternity and Neonatology, Tunisia.
Ines Zouari4 Centre of Maternity and Neonatology, Tunisia.
Raja El Faleh4 Centre of Maternity and Neonatology, Tunisia.
Jean Guibourdenche3 INSERM UMR-S1139 College of Pharmacy, Paris Descartes University, France.
Wassim Y Almawi5 Faculty of Science of Tunis, University of Tunis El Manar, Tunisia.
Touhami Mahjoub1 Laboratory of Human Genome and Multifactorial Diseases (LR12ES07), College of Pharmacy, University of Monastir, Tunisia.
University of Carthage · TNUniversity of Monastir · TNTunis University · TNUniversité Paris Cité · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPreeclampsia (PE) is a pregnancy-associated hypertensive disorder and a leading cause of maternal and neonatal morbidity and mortality. While its pathogenesis remains ill defined, several candidate genes for PE have been identified, but results remain inconclusive. We investigated the association of the angiotensinogen ( AGT) gene variants M235T and T174M with PE, and we analyzed the contribution of both variants to the severity of PE.

methodsThis case-control study enrolled 550 Tunisian pregnant women: 272 with PE, of whom 147 presented with mild, and 125 with severe PE, along with 278 unrelated age- and ethnically matched control women. AGT genotyping was performed by polymerase chain reaction-restriction fragment length polymorphism.

resultsSignificantly higher M235T minor allele frequency (MAF) was associated with increased risk of PE ( p < 0.001). Decreased frequency of heterozygous T174M genotype carriers were found in control women ( p = 0.015), suggesting a protective effect of this genotype (odds ratio (95% confidence interval) = 0.51 (0.29-0.89)). Two-locus haplotype analysis demonstrated MM and TT haplotypes to be negatively and positively associated with PE, respectively. MAF of M253T, but not T174M, was higher in the severe PE group, and carrying M235T or T174M minor allele was associated with increased body mass index ( p < 0.001) among unselected PE women.

conclusionsAGT M235T and T174M variants contribute to an increased risk of developing PE, and for M235T to PE severity.

Indexed as

Genetic Predisposition to DiseaseSeverity of Illness IndexAdultAllelesAngiotensinogenCase-Control StudiesFemaleHaplotypesHumansPolymorphism, Single NucleotidePre-EclampsiaPregnancyTunisiaAngiotensinogenangiotensinogenhaplotypepolymorphismPreeclampsiasevere preeclampsia

Identifiers

PMID29366364
PMCPMC5843851
OpenAlexW2790387310

What OpenQuestion holds

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LicenceCC BY-NC
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Registered trials

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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.