Evidence map›Paper›PMID 30400060›Full record

ReviewJournal of molecular endocrinology2019

Nutrient sensor signaling pathways and cellular stress in fetal growth restriction.

Bethany Hart, Elizabeth Morgan, Emilyn U Alejandro

Open access · bronzeAbstract readReview
In one paragraph

Review in Journal of molecular endocrinology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed, 1 pooled it
8.0field-weighted citation impact, top 3% 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

41 citing papers in PubMed, 1 synthesis or guideline pooled it, 104 citations in OpenAlex.

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  15. A multi-organ analysis of the role of mTOR in fetal alcohol spectrum disorders.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023
    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 1 institution in 1 country.

Bethany HartDivision of Maternal-Fetal Medicine, Department of Obstetrics, Gynecology, and Women's Health, University of Minnesota, Minneapolis, Minnesota, USA.
Elizabeth MorganDivision of Maternal-Fetal Medicine, Department of Obstetrics, Gynecology, and Women's Health, University of Minnesota, Minneapolis, Minnesota, USA.
Emilyn U AlejandroDepartment of Integrative Biology and Physiology, University of Minnesota, Minneapolis, Minnesota, USA.
University of Minnesota · US

Funding

The role of O-linked N-Acetylglucosamine Homeostasis in Pancreatic Beta-cell Development and FunctionR01DK115720 · NIDDK · UNIVERSITY OF MINNESOTA · PI ALEJANDRO, EMILYN · 2018 to 2022
$1.9M
O-linked-N-acetylglucosamine Post-translational Modification in Pancreatic Beta-cells Regulating ER Stress and Mitochondrial FunctionR21DK112144 · NIDDK · UNIVERSITY OF MINNESOTA · PI ALEJANDRO, EMILYN · 2017 to 2019
$576k
Mechanisms of Developmental Programing of beta-cell Susceptibility to GlucolipotoxicityK01DK103823 · NIDDK · UNIVERSITY OF MINNESOTA · PI ALEJANDRO, EMILYN · 2014 to 2017
$572k
Role of placental nutrient-sensor protein mTOR on fetal programming of beta-cell dysfunction and susceptibility to type 2 diabetesR03DK114465 · NIDDK · UNIVERSITY OF MINNESOTA · PI ALEJANDRO, EMILYN · 2018 to 2019
$360k
NIDDK NIH HHS K01 DK103823NIDDK NIH HHS R01 DK115720NIDDK NIH HHS R03 DK114465NIDDK NIH HHS R21 DK112144
6 · The paper itself

Abstract

Fetal growth restriction is one of the most common obstetrical complications resulting in significant perinatal morbidity and mortality. The most frequent etiology of human singleton fetal growth restriction is placental insufficiency, which occurs secondary to reduced utero-placental perfusion, abnormal placentation, impaired trophoblast invasion and spiral artery remodeling, resulting in altered nutrient and oxygen transport. Two nutrient-sensing proteins involved in placental development and glucose and amino acid transport are mechanistic target of rapamycin (mTOR) and O-linked N-acetylglucosamine transferase (OGT), which are both regulated by availability of oxygen. Impairment in either of these pathways is associated with fetal growth restriction and accompanied by cellular stress in the forms of hypoxia, oxidative and endoplasmic reticulum (ER) stress, metabolic dysfunction and nutrient starvation in the placenta. Recent evidence has emerged regarding the potential impact of nutrient sensors on fetal stress response, which occurs in a sexual dysmorphic manner, indicating a potential element of genetic gender susceptibility to fetal growth restriction. In this mini review, we focus on the known role of mTOR and OGT in placental development, nutrient regulation and response to cellular stress in human fetal growth restriction with supporting evidence from rodent models.

Indexed as

Signal TransductionStress, PhysiologicalAnimalsFemaleFetal Growth RetardationHumansMaleNutrientsPlacentaPregnancySex CharacteristicsNutrientscellular stressfetal growth restrictionmTORnutrient sensorsnutrient transportO-GlcNAc transferase (OGT)placentasexual dymorphism

Identifiers

PMID30400060
PMCPMC6443503
OpenAlexW2897165847

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.