Evidence map›Paper›PMID 33402454›Full record

ReviewIn vivo (Athens, Greece)

The Angiotensin-converting Enzyme Insertion/Deletion Polymorphism as a Common Risk Factor for Major Pregnancy Complications.

Iphigenia Gintoni, Maria Adamopoulou, Christos Yapijakis

Open access · diamondAbstract readReview
In one paragraph

Review in In vivo (Athens, Greece). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
3.0field-weighted citation impact, top 8% 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

14 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. The Impact ofIn vivo (Athens, Greece)
    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

3 authors at 2 institutions in 1 country.

Iphigenia GintoniUnit of Orofacial Genetics, 1 Department of Paediatrics, School of Medicine, "Agia Sophia" Children's Hospital, National Kapodistrian University of Athens, Athens, Greece.
Maria AdamopoulouDepartment of Biomedical Sciences, University of West Attica, Athens, Greece.
Christos Yapijakis *Unit of Orofacial Genetics, 1 Department of Paediatrics, School of Medicine, "Agia Sophia" Children's Hospital, National Kapodistrian University of Athens, Athens, Greece; cyapi@med.uoa.gr.
National and Kapodistrian University of Athens · GRUniversity of West Attica · GR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Idiopathic pregnancy complications pose a major threat to both maternal and fetal health worldwide. Numerous studies have implicated the role of the renin-angiotensin system (RAS) in the development of obstetric syndromes, since it is crucial for the uteroplacental function. A major RAS component is the angiotensin-converting enzyme (ACE), which hydrolyses angiotensin I to angiotensin II, and not only regulates arterial pressure, but also fibrinolytic activity, indirectly, through the expression of plasminogen activator inhibitor-1. A key functional polymorphism of the ACE gene is the insertion/deletion (I/D) polymorphism, which affects gene expression and product levels, and can therefore lead to high blood pressure and/or reduced fibrinolytic activity. These can cause major pregnancy complications, such as preeclampsia, recurrent pregnancy loss and preterm birth. This review discusses how the ACE I/D is associated with susceptibility towards pregnancy complications, on its own or in combination with other functional gene polymorphisms such, as the angiotensin II receptor type 1 (AT1R) A1166CC, angiotensin II receptor type 2 (AT2R) G1332A, plasminogen activator inhibitor-1 (PAI-1) 4G/5G, matrix metallopeptidase-9 (MMP-9) C1562T, angiotensinogen (AGT) M235T, renin (REN) 83A/G, factor XIII (F13) Val34Leu and endothelial nitric oxide synthase (eNOS) 4a/b.

Indexed as

Pre-EclampsiaPremature BirthFemaleGenotypeHumansInfant, NewbornPeptidyl-Dipeptidase APolymorphism, GeneticPregnancyRenin-Angiotensin SystemRisk FactorsPeptidyl-Dipeptidase AACEmiscarriageobstetrical complicationspreeclampsiapregnancy losspreterm birthrenin-angiotensin systemreview

Identifiers

PMID33402454
PMCPMC7880778
OpenAlexW3119811193

What OpenQuestion holds

Textmetadata
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.