Evidence map›Paper›PMID 21547091›Full record

ReviewJournal of pregnancy2011

The role of placental homeobox genes in human fetal growth restriction.

Padma Murthi, Gayathri Rajaraman, Shaun Patrick Brennecke, Bill Kalionis

Open access · goldAbstract readReview
In one paragraph

Review in Journal of pregnancy, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.9field-weighted citation impact, top 23% 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

7 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
  2. AdaptiveiScience · 2025
    Article
  3. Article
  4. The Update of Fetal Growth Restriction Associated with Biomarkers.Maternal-fetal medicine (Wolters Kluwer Health, Inc.) · 2022
    Review
  5. Article
  6. Article
  7. Article
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

4 authors at 2 institutions in 1 country.

Padma MurthiDepartment of Obstetrics and Gynaecology, The University of Melbourne, Melbourne, Victoria 3010, Australia; Pregnancy Research Centre, Department of Perinatal Medicine, Royal Women's Hospital, Parkville, Victoria 3052, Australia. padma@unimelb.edu.au
Gayathri Rajaraman
Shaun Patrick Brennecke
Bill Kalionis
Royal Women's Hospital · AUUniversity of Melbourne · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fetal growth restriction (FGR) is an adverse pregnancy outcome associated with significant perinatal and paediatric morbidity and mortality, and an increased risk of chronic disease later in adult life. One of the key causes of adverse pregnancy outcome is fetal growth restriction (FGR). While a number of maternal, fetal, and environmental factors are known causes of FGR, the majority of FGR cases remain idiopathic. These idiopathic FGR pregnancies are frequently associated with placental insufficiency, possibly as a result of placental maldevelopment. Understanding the molecular mechanisms of abnormal placental development in idiopathic FGR is, therefore, of increasing importance. Here, we review our understanding of transcriptional control of normal placental development and abnormal placental development associated with human idiopathic FGR. We also assess the potential for understanding transcriptional control as a means for revealing new molecular targets for the detection, diagnosis, and clinical management of idiopathic FGR.

Indexed as

FemaleFetal Growth RetardationGene Expression RegulationHomeodomain ProteinsHumansPlacentaPlacental InsufficiencyPregnancyTranscription, GeneticHomeodomain Proteins

Identifiers

PMID21547091
PMCPMC3087155
OpenAlexW1994461680

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.