Evidence map›Paper›PMID 35493783›Full record

ArticleAnimal reproduction2022

Rodent models in placental research. Implications for fetal origins of adult disease.

Nicole Aguilera, Francisca Salas-Pérez, Macarena Ortíz, Daniela Álvarez, Bárbara Echiburú, Manuel Maliqueo

Open access · goldAbstract read
In one paragraph

Article in Animal reproduction, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
9.5field-weighted citation impact, top 2% 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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.

  1. Pooled it
  2. Review
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  5. Review
  6. Article
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  18. Therapeutic potential of extracellular vesicles for treating human pregnancy disorders.Extracellular vesicles and circulating nucleic acids · 2025
    Review
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  20. In vitro effect of vitaminBToxicology research · 2024
    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

6 authors at 2 institutions in 1 country.

Nicole AguileraLaboratorio de Endocrinología y Metabolismo, Facultad de Medicina Occidente, Universidad de Chile, Santiago, Chile.ORCID 0000-0002-8542-7753
Francisca Salas-PérezLaboratorio de Endocrinología y Metabolismo, Facultad de Medicina Occidente, Universidad de Chile, Santiago, Chile.ORCID 0000-0002-9974-8443
Macarena OrtízLaboratorio de Endocrinología y Metabolismo, Facultad de Medicina Occidente, Universidad de Chile, Santiago, Chile.ORCID 0000-0002-8243-8158
Daniela ÁlvarezLaboratorio de Endocrinología y Metabolismo, Facultad de Medicina Occidente, Universidad de Chile, Santiago, Chile.ORCID 0000-0002-1719-5698
Bárbara EchiburúLaboratorio de Endocrinología y Metabolismo, Facultad de Medicina Occidente, Universidad de Chile, Santiago, Chile.ORCID 0000-0001-6535-3104
Manuel MaliqueoLaboratorio de Endocrinología y Metabolismo, Facultad de Medicina Occidente, Universidad de Chile, Santiago, Chile.ORCID 0000-0003-3872-0217
University of Chile · CLUniversidad Bernardo O'Higgins · CL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Rodent models in rats, mice, and guinea pigs have been extremely helpful to gain insight into pregnancy physiology and pathologies-related. Moreover, they have allowed understanding the mechanism that links an adverse intrauterine environment with the origin of adult disease. In this regard, the effects of diverse maternal conditions, such as undernutrition, obesity, hypoxia, and hyperandrogenism on placental function and its long-term consequences for the offspring, have been widely analyzed through rodents models involving dietary manipulations, modifications in environmental oxygen, surgical and pharmacological procedures that reduce uteroplacental blood flow and administrations of exogenous testosterone and dihydrotestosterone (DHT) mimicking maternal androgen excess. Both in human and in rodent models, these interventions induce modifications of placental morphology, transport of glucose, amino acid, and fatty acids, steroid synthesis, and signaling pathways control placental function. These changes are associated with the increase of pro-inflammatory and oxidative stress markers. For its part, offspring exhibit alterations in organs involved in metabolic control such as the hypothalamus, adipose tissue, liver, skeletal muscle, and pancreas altering the intake and preferences for certain foods, the metabolism of glucose and lipid, and hormonal function leading to fat accumulation, insulin resistance, fatty liver, dyslipidemia, and elevated glucose levels. Therefore, the present review discusses the evidence emerging from rodent models that relate maternal nutrition, hypoxia, and androgen exposure to the maternal mechanisms that lead to fetal programming and their metabolic consequences in postnatal life.

Indexed as

and hyperandrogenismhypoxiamaternal nutritionrodent models

Identifiers

PMID35493783
PMCPMC9037606
OpenAlexW4225947974

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.