Evidence map›Paper›PMID 30085007›Full record

ArticleBiology of reproduction2019

Sexual dimorphism of mitochondrial function in the hypoxic guinea pig placenta.

Hong Song, Bhanu P Telugu, Loren P Thompson

Open access · bronzeAbstract read
In one paragraph

Article in Biology of reproduction, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

22 citing papers in PubMed, 34 citations in OpenAlex.

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  14. Placental mitochondrial dysfunction with metabolic diseases: Therapeutic approaches.Biochimica et biophysica acta. Molecular basis of disease · 2021
    Review
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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

3 authors at 2 institutions in 1 country.

Hong SongDepartment of Obstetrics, Gynecology and Reproductive Sciences, University of Maryland School of Medicine, Baltimore, Maryland, USA.
Bhanu P TeluguAnimal Biosciences and Biotechnology Laboratory, USDA-ARS, Beltsville, Maryland, USA.
Loren P ThompsonDepartment of Obstetrics, Gynecology and Reproductive Sciences, University of Maryland School of Medicine, Baltimore, Maryland, USA.
University of Maryland, Baltimore · USBeltsville Agricultural Research Center · US

Funding

Impact of Prenatal Hypoxia on Mitochondrial Function of Offspring HeartsR01HL126859 · NHLBI · UNIVERSITY OF MARYLAND BALTIMORE · PI ALBRECHT, EUGENE D. · 2015 to 2022
$3.7M
NHLBI NIH HHS R01 HL126859NHLBI NIH HHS R56 HL126859
6 · The paper itself

Abstract

Placental hypoxia can stimulate oxidative stress and mitochondrial dysfunction reducing placental efficiency and inducing fetal growth restriction (FGR). We hypothesized that chronic hypoxia inhibits mitochondrial function in the placenta as an underlying cause of cellular mechanisms contributing to FGR. Pregnant guinea pigs were exposed to either normoxia (NMX) or hypoxia (HPX; 10.5% O2) at 25 day gestation until term (65 day). Guinea pigs were anesthetized, and fetuses and placentas were excised at either mid (40 day) or late gestation (64 day), weighed, and placental tissue stored at -80°C until assayed. Mitochondrial DNA content, protein expression of respiratory Complexes I-V, and nitration and activity rates of Complexes I and IV were measured in NMX and HPX male (N = 6 in each treatment) and female (N = 6 in each treatment) placentas. Mitochondrial density was not altered by HPX in either mid- or late-term placentas. In mid gestation, HPX slightly increased expression of Complexes I-III and V in male placentas only, but had no effect on either Complex I or IV activity rates or nitrotyrosine expression. In late gestation, HPX significantly decreased CI/CIV activity rates and increased CI/CIV nitration in male but not female placentas exhibiting a sexual dimorphism. Complex I-V expression was reduced from mid to late gestation in both male and female placentas regardless of treatment. We conclude that chronic HPX decreases mitochondrial function by inhibiting Complex I/IV activity via increased peroxynitrite in a sex-related manner. Further, there may be a progressive decrease in energy metabolism of placental cell types with gestation that increases the vulnerability of placental function to intrauterine stress.

Indexed as

Prenatal Exposure Delayed EffectsSex CharacteristicsAnimalsDNA, MitochondrialFemaleFetal Growth RetardationFetal HypoxiaFetal WeightHypoxiaMaleMitochondriaOrgan SizeOxidative StressPlacentaPregnancyDNA, Mitochondrial

Identifiers

PMID30085007
PMCPMC6335207
OpenAlexW2887523569

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.