{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,12]],"date-time":"2026-10-12T21:10:41Z","timestamp":1791839441641,"version":"4.3.4"},"reference-count":238,"publisher":"Bioscientifica","issue":"2","content-domain":{"domain":["jme.bioscientifica.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2019,2]]},"abstract":"<jats:p>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.<\/jats:p>","DOI":"10.1530\/jme-18-0059","type":"journal-article","created":{"date-parts":[[2018,10,10]],"date-time":"2018-10-10T10:42:09Z","timestamp":1539168129000},"page":"R155-R165","update-policy":"https:\/\/doi.org\/10.1530\/crossmarkpolicy-6","source":"Crossref","is-referenced-by-count":69,"title":["Nutrient sensor signaling pathways and cellular stress in fetal growth restriction"],"prefix":"10.1530","volume":"62","author":[{"given":"Bethany","family":"Hart","sequence":"first","affiliation":[{"name":"1Division of Maternal-Fetal Medicine, Department of Obstetrics, Gynecology, and Women\u2019s Health, University of Minnesota, Minneapolis, Minnesota, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elizabeth","family":"Morgan","sequence":"additional","affiliation":[{"name":"1Division of Maternal-Fetal Medicine, Department of Obstetrics, Gynecology, and Women\u2019s Health, University of Minnesota, Minneapolis, Minnesota, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Emilyn U","family":"Alejandro","sequence":"additional","affiliation":[{"name":"2Department of Integrative Biology and Physiology, University of Minnesota, Minneapolis, Minnesota, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"416","reference":[{"key":"ref251","doi-asserted-by":"crossref","first-page":"303","DOI":"10.1159\/000366079","article-title":"Mitochondrial DNA in placenta: associations with fetal growth and superoxide dismutase activity","volume":"82","year":"2014a","journal-title":"Hormone Research in Paediatrics"},{"key":"ref1291","doi-asserted-by":"crossref","first-page":"2893","DOI":"10.1101\/gad.1256804","article-title":"Regulation of mTOR function in response to hypoxia by REDD1 and the TSC1\/TSC2 tumor suppressor complex","volume":"18","year":"2004","journal-title":"Genes and Development"},{"key":"ref1571","doi-asserted-by":"crossref","first-page":"1017","DOI":"10.1038\/nature05815","article-title":"Cycling of O-linked beta-N-acetylglucosamine on nucleocytoplasmic proteins","volume":"446","year":"2007","journal-title":"Nature"},{"key":"ref2221","doi-asserted-by":"crossref","first-page":"1047","DOI":"10.1111\/j.1447-0756.2009.01063.x","article-title":"Serum prolidase activity and oxidative stress markers in pregnancies with intrauterine growth restricted infants","volume":"35","year":"2009","journal-title":"Journal of Obstetrics and Gynaecology Research"},{"key":"ref2271","first-page":"293271","article-title":"Oxidative stress in placenta: health and diseases","volume":"2015","year":"2015","journal-title":"BioMed Research International"},{"key":"ref221","doi-asserted-by":"crossref","first-page":"A5","DOI":"10.1016\/j.placenta.2015.07.199","article-title":"Maternal corticosterone exposure in the mouse causes sex specific alterations in placental OGT and O-linked glycosylation","volume":"36","year":"2015","journal-title":"Placenta"},{"key":"ref2261","doi-asserted-by":"crossref","first-page":"435","DOI":"10.1016\/S0006-291X(03)00175-X","article-title":"O-GlcNAc: a regulatory post-translational modification","volume":"302","year":"2003","journal-title":"Biochemical and Biophysical Research Communications"},{"key":"ref1061","doi-asserted-by":"crossref","first-page":"32","DOI":"10.1186\/s13041-017-0311-1","article-title":"O-GlcNAc regulation of autophagy and alpha-synuclein homeostasis; 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