Evidence map›Paper›PMID 22687819›Full record

ReviewPlacenta2012

The emerging role of mTORC1 signaling in placental nutrient-sensing.

T Jansson, I L M H Aye, D C I Goberdhan

Open access · greenAbstract readReview
In one paragraph

Review in Placenta, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.

0numbers the graph read from it
0cells of the map it votes in
78citing papers in PubMed
8.1field-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

78 citing papers in PubMed, 161 citations in OpenAlex.

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18 more citing papers are in PubMed but not listed here.

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 2 countries.

T JanssonCenter for Pregnancy and Newborn Research, Department of OB/GYN, University of Texas Health Science Center, Mail Code 7836, 7703 Floyd Curl Drive, San Antonio, TX 78229-3900, USA. jansson@uthscsa.edu
I L M H Aye
D C I Goberdhan
The University of Texas Health Science Center at San Antonio · USUniversity of Oxford · GB

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
Molecular Mechanisms Linking Placental Nutrient Sensing and Fetal ProgrammingR21HD071306 · NICHD · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI MYATT, LESLIE · 2012 to 2013
$378k
Cancer Research UK C38302/A12278NICHD NIH HHS HD 068370NICHD NIH HHS R01 HD068370NICHD NIH HHS R21 HD071306
6 · The paper itself

Abstract

Nutrient-sensing signaling pathways regulate cell metabolism and growth in response to altered nutrient levels and growth factor signaling. Because trophoblast cell metabolism and associated signaling influence fetal nutrient availability, trophoblast nutrient sensors may have a unique role in regulating fetal growth. We review data in support of a role for mammalian target of rapamycin complex 1 (mTORC1) in placental nutrient-sensing. Placental insulin/IGF-I signaling and fetal levels of oxygen, glucose and amino acids (AAs) are altered in pregnancy complications such as intrauterine growth restriction, and all these factors are well-established upstream regulators of mTORC1. Furthermore, mTORC1 is a positive regulator of placental AA transporters, suggesting that trophoblast mTORC1 modulates AA transfer across the placenta. In addition, placental mTORC1 signaling is also known to be modulated in pregnancy complications associated with altered fetal growth and in animal models in which maternal nutrient availability has been altered experimentally. Recently, significant progress has been made in identifying the molecular mechanisms by which mTORC1 senses AAs, a process requiring shuttling of mTOR to late endosomal and lysosomal compartments (LELs). We recently identified members of the proton-assisted amino acid transporter (PAT/SLC36) family as critical components of the AA-sensing system or 'nutrisome' that regulates mTORC1 on LEL membranes, placing AA transporters and their subcellular regulation both upstream and downstream of mTORC1-driven processes. We propose a model in which placental mTORC1 signaling constitutes a critical link between maternal nutrient availability and fetal growth, thereby influencing the long-term health of the fetus.

Indexed as

Amino AcidsAmino Acid Transport SystemsAnimalsFemaleFetal Growth RetardationHumansMaternal-Fetal ExchangeMechanistic Target of Rapamycin Complex 1Multiprotein ComplexesPlacentaPregnancyPregnancy ComplicationsPrenatal Nutritional Physiological PhenomenaSignal TransductionTOR Serine-Threonine KinasesTrophoblastsAmino AcidsAmino Acid Transport SystemsMechanistic Target of Rapamycin Complex 1Multiprotein ComplexesTOR Serine-Threonine Kinases

Identifiers

PMID22687819
PMCPMC3463762
OpenAlexW1974323903

What OpenQuestion holds

Textmetadata
LicenceTDM
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.