Evidence map›Paper›PMID 30476008›Full record

ReviewBiology of reproduction2019

Novel roles of mechanistic target of rapamycin signaling in regulating fetal growth†.

Madhulika B Gupta, Thomas Jansson

Open access · bronzeAbstract readReview
In one paragraph

Review 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 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

37 citing papers in PubMed, 67 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Article
  6. Maternal Adiponectin Decreases Placenta Nutrient Transport in Mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Effects ofEnvironmental science & technology · 2023
    Article
  18. Review
  19. Article
  20. Article
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

2 authors at 2 institutions in 2 countries.

Madhulika B GuptaDepartment of Pediatrics, University of Western Ontario, London, Ontario, Canada.
Thomas JanssonDepartment of Obstetrics and Gynecology, Division of Reproductive Sciences, University of Colorado | Anschutz Medical Campus, Aurora, Colorado, USA.
University of Colorado Anschutz Medical Campus · USWestern University · CA

Funding

PARTURITION AND FETAL PRIMATE HYPOTHALAMIC FUNCTIONP01HD021350 · NICHD · UNIVERSITY OF WYOMING · PI NATHANIELSZ, PETER W. · 1987 to 2018
$19.9M
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
Placental adiponectin signaling and fetal programming in maternal obesityR01HD065007 · NICHD · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI JANSSON, THOMAS, POWELL, THERESA L · 2011 to 2022
$3.8M
mTOR as a trophoblast folate sensorR01HD078376 · NICHD · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI JANSSON, THOMAS · 2014 to 2018
$1.6M
Decidual nutrient sensing and IGFBP-1 phosphorylation in placental insufficiencyR01HD089980 · NICHD · UNIVERSITY OF COLORADO DENVER · PI GUPTA, MADHULIKA, JANSSON, THOMAS · 2017 to 2021
$1.4M
NICHD NIH HHS P01 HD021350NICHD NIH HHS R01 HD065007NICHD NIH HHS R01 HD068370NICHD NIH HHS R01 HD078376NICHD NIH HHS R01 HD089980
6 · The paper itself

Abstract

Mechanistic target of rapamycin (mTOR) signaling functions as a central regulator of cellular metabolism, growth, and survival in response to hormones, growth factors, nutrients, energy, and stress signals. Mechanistic TOR is therefore critical for the growth of most fetal organs, and global mTOR deletion is embryonic lethal. This review discusses emerging evidence suggesting that mTOR signaling also has a role as a critical hub in the overall homeostatic control of fetal growth, adjusting the fetal growth trajectory according to the ability of the maternal supply line to support fetal growth. In the fetus, liver mTOR governs the secretion and phosphorylation of insulin-like growth factor binding protein 1 (IGFBP-1) thereby controlling the bioavailability of insulin-like growth factors (IGF-I and IGF-II), which function as important growth hormones during fetal life. In the placenta, mTOR responds to a large number of growth-related signals, including amino acids, glucose, oxygen, folate, and growth factors, to regulate trophoblast mitochondrial respiration, nutrient transport, and protein synthesis, thereby influencing fetal growth. In the maternal compartment, mTOR is an integral part of a decidual nutrient sensor which links oxygen and nutrient availability to the phosphorylation of IGFBP-1 with preferential effects on the bioavailability of IGF-I in the maternal-fetal interface and in the maternal circulation. These new roles of mTOR signaling in the regulation fetal growth will help us better understand the molecular underpinnings of abnormal fetal growth, such as intrauterine growth restriction and fetal overgrowth, and may represent novel avenues for diagnostics and intervention in important pregnancy complications.

Indexed as

AnimalsFemaleFetal DevelopmentFetal Growth RetardationFetal MacrosomiaHumansInsulin-Like Growth Factor IPlacentaPregnancySignal TransductionTOR Serine-Threonine KinasesInsulin-Like Growth Factor IMTOR protein, humanTOR Serine-Threonine Kinasesdeciduadevelopmental origins of health and diseasefetal developmentinsulin-like growth factorintrauterine growth restrictionkinasesmetabolismnutritionplacentaplacental transportpregnancysyncytiotrophoblast

Identifiers

PMID30476008
PMCPMC6698747
OpenAlexW2901283446

What Socratic 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 Socratic graph.