Evidence map›Paper›PMID 41265498›Full record

ArticleFree radical biology & medicine2026

Placental mitochondrial respiration is inhibited in mice with trophoblast specific AdipoR2 overexpression.

Hiroshi Shimada, Toshihide Sakuragi, Kenneth Barentsen, Kathryn Erickson, Johann Urschitz, Theresa L Powell, Thomas Jansson, Fredrick J Rosario

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Article in Free radical biology & medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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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

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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

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0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

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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

8 authors.

Hiroshi ShimadaDepartment of Obstetrics and Gynecology, University of Colorado, Anschutz Medical Campus, Aurora, CO, USA; Department of Obstetrics & Gynecology, Sapporo Medical University, Sapporo, Japan.
Toshihide SakuragiDepartment of Obstetrics and Gynecology, University of Colorado, Anschutz Medical Campus, Aurora, CO, USA; Department of Obstetrics & Gynecology, University of Occupational and Environmental Health, Japan.
Kenneth BarentsenDepartment of Obstetrics and Gynecology, University of Colorado, Anschutz Medical Campus, Aurora, CO, USA.
Kathryn EricksonDepartment of Obstetrics and Gynecology, University of Colorado, Anschutz Medical Campus, Aurora, CO, USA; Department of Pediatrics, University of Colorado, Anschutz Medical Campus, Aurora, CO, USA.
Johann UrschitzYanagimachi Institute for Biogenesis Research, University of Hawaii, Honolulu, HI, USA.
Theresa L PowellDepartment of Obstetrics and Gynecology, University of Colorado, Anschutz Medical Campus, Aurora, CO, USA; Department of Pediatrics, University of Colorado, Anschutz Medical Campus, Aurora, CO, USA.
Thomas JanssonDepartment of Obstetrics and Gynecology, University of Colorado, Anschutz Medical Campus, Aurora, CO, USA.
Fredrick J RosarioDepartment of Obstetrics and Gynecology, University of Colorado, Anschutz Medical Campus, Aurora, CO, USA. Electronic address: fredrick.joseph@cuanschutz.edu.

Funding

Trophoblast mTOR: a critical hub linking maternal nutrient supply to placental function, fetal growth and fetal islet functionR01HD068370 · NICHD · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI JANSSON, THOMAS, ROSARIO-JOSEPH, FREDRICK · 2011 to 2024
$4.1M
Development of approaches for inducible trophoblast-specific gene modulation: the role of trophoblast Lat1 in the regulation of placental function and fetal growthR01HD105701 · NICHD · UNIVERSITY OF COLORADO DENVER · PI Thomas L Brown, Thomas Jansson · 2023 to 2026
$2.6M
NICHD NIH HHS R01 HD068370NICHD NIH HHS R01 HD105701
6 · The paper itself

Abstract

Maternal circulating levels of adiponectin are inversely correlated with fetal growth mediated by its effect on placental function. The cellular effects of adiponectin on trophoblast are mainly mediated by adiponectin receptor isoform 2 (AdipoR2) resulting in the activation of PPARα and synthesis of ceramides, which inhibit insulin and mTOR signaling. We have recently demonstrated that trophoblast-specific overexpression of AdipoR2 in pregnant mice inhibits placental mTORC1 signaling and nutrient transport, resulting in fetal growth restriction. Trophoblast mTORC1 signaling is a positive regulator of mitochondrial respiration. However, it is unknown if placental adiponectin signaling is mechanistically linked to mitochondrial function. We hypothesized that trophoblast-specific overexpression of AdipoR2 in pregnant mice decreases placental oxidative phosphorylation. At Embryonic day (E) 3.5, blastocysts from super-ovulated, time-mated B6D2F1 female mice were collected and transduced with lentivirus constructs for AdipoR2-overexpression (AdipoR2-OX) or scramble (SCR) sequences. The blastocysts were surgically transferred to pseudo-pregnant CD-1 recipient dams. Following euthanasia at E18.5, we separated the labyrinth and the junctional zone. In the labyrinth, AdipoR2 overexpression significantly inhibited placental mitochondrial GMP

Indexed as

MitochondriaPlacentaReceptors, AdiponectinTrophoblastsAdiponectinAnimalsCell RespirationFemaleMechanistic Target of Rapamycin Complex 1MiceMultiprotein ComplexesOxidative PhosphorylationPregnancySignal TransductionTOR Serine-Threonine KinasesAdiponectinadiponectin receptor 2, mouseMechanistic Target of Rapamycin Complex 1Multiprotein ComplexesReceptors, AdiponectinTOR Serine-Threonine KinasesAdiponectinCell respirationFetal developmentMaternal-fetal exchangePregnancy

Identifiers

PMID41265498
PMCPMC13492874

What Socratic holds

Textmetadata
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Registered trials

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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 Socratic graph.