Evidence map›Paper›PMID 35293971›Full record

ArticleBiology of reproduction2022

Placental structure, function, and mitochondrial phenotype relate to fetal size in each fetal sex in mice†.

Esteban Salazar-Petres, Daniela Pereira-Carvalho, Jorge Lopez-Tello, Amanda Nancy Sferruzzi-Perri

Open access · hybridAbstract read
In one paragraph

Article in Biology of reproduction, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
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

20 citing papers in PubMed, 25 citations in OpenAlex.

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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

4 authors at 2 institutions in 1 country.

Esteban Salazar-PetresDepartment of Physiology, Development and Neuroscience, Centre for Trophoblast Research, University of Cambridge, Cambridge, UK.
Daniela Pereira-CarvalhoDepartment of Physiology, Development and Neuroscience, Centre for Trophoblast Research, University of Cambridge, Cambridge, UK.
Jorge Lopez-TelloDepartment of Physiology, Development and Neuroscience, Centre for Trophoblast Research, University of Cambridge, Cambridge, UK.
Amanda Nancy Sferruzzi-PerriDepartment of Physiology, Development and Neuroscience, Centre for Trophoblast Research, University of Cambridge, Cambridge, UK.
University of Cambridge · GBOxford Centre for Computational Neuroscience · GB

Funding

Medical Research Council MR/R022690/1Medical Research Council MR/R022690/1/RG93186Wellcome TrustWellcome Trust 220456/Z/20/Z
6 · The paper itself

Abstract

Fetal growth depends on placental function, which requires energy from mitochondria. Here we investigated whether mitochondrial function in the placenta relates to the growth of the lightest and heaviest fetuses of each sex within the litter of mice. Placentas from the lightest and heaviest fetuses were taken to evaluate placenta morphology (stereology), mitochondrial energetics (high-resolution respirometry), mitochondrial regulators, nutrient transporters, hormone handling, and signaling pathways (qPCR and Western blotting). We found that mitochondrial complex I and II oxygen consumption rate was greater for placentas supporting the lightest female fetuses, although placental complex I abundance of the lightest females and complexes III and V of the lightest males were decreased compared to their heaviest counterparts. Expression of mitochondrial biogenesis (Nrf1) and fission (Drp1 and Fis1) genes was lower in the placenta from the lightest females, whilst biogenesis-related gene Tfam was greater in the placenta of the lightest male fetuses. In addition, placental morphology and steroidogenic gene (Cyp17a1 and Cyp11a1) expression were aberrant for the lightest females, but glucose transporter (Slc2a1) expression was lower in only the lightest males versus their heaviest counterparts. Differences in intra-litter placental phenotype were related to changes in the expression of hormone-responsive (androgen receptor) and metabolic signaling (AMPK, AKT, and PPARγ) pathways. Thus, in normal mouse pregnancy, placental structure, function, and mitochondrial phenotype are differentially responsive to the growth of the female and male fetus. This study may inform the design of sex-specific therapies for placental insufficiency and fetal growth abnormalities with life-long benefits for the offspring.

Indexed as

Fetal DevelopmentPlacentaAnimalsFemaleHormonesMaleMiceMitochondriaPhenotypePregnancyHormonesfetushormonesmitochondriaplacentasextransport

Identifiers

PMID35293971
PMCPMC9327737
OpenAlexW4221008345

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.