ArticleClinical science (London, England : 1979)2021
Placenta-specific Slc38a2/SNAT2 knockdown causes fetal growth restriction in mice.
Article in Clinical science (London, England : 1979), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
What it found
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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.
The trial behind it
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Who cites it
35 citing papers in PubMed, 44 citations in OpenAlex.
- The Role of Branched-Chain Amino Acids in Nutrient Allocation of the Porcine Placenta: A Review.Animals : an open access journal from MDPI · 2026Review
- Sexual Dimorphism in Placental mTORC1 Signaling, Amino Acid Transport, and Mitochondrial Respiration at Term.Antioxidants (Basel, Switzerland) · 2026Article
- Metabolic imprinting in trophoblast barrier dysfunction: the role of glucolipotoxicity, endoplasmic reticulum stress, and amino acid transport imbalance.Journal of assisted reproduction and genetics · 2026Review
- Placental mitochondrial respiration is inhibited in mice with trophoblast specific AdipoR2 overexpression.Free radical biology & medicine · 2026Article
- Folic acid ameliorates placental structure and function in fetal growth restriction via epigenetic modifications.Clinical epigenetics · 2025Article
- Novel role for PI3Kβ in placental function through regulation of system A amino acid transporter expression, associated with embryonic lethality.Cellular and molecular life sciences : CMLS · 2025Article
- Normalization of trophoblast mTOR signaling rescues impaired function in primary human trophoblast cells isolated from pregnancies complicated by fetal growth restriction.Cell death discovery · 2025Article
- PiggyBac transposase-mediated inducible trophoblast-specific knockdown of Mtor decreases placental nutrient transport and fetal growth.Clinical science (London, England : 1979) · 2025Article
- Placental Protein Citrullination Signatures Are Modified in Early- and Late-Onset Fetal Growth Restriction.International journal of molecular sciences · 2025Article
- Trophoblast-specific Deptor knockdown enhances trophoblast nutrient transport and fetal growth in mice.Acta physiologica (Oxford, England) · 2025Article
- Lentivirus-Mediated Trophoblast-Specific Deptor Knockdown Increases Transplacental System A and System L Amino Acid Transport and Fetal Growth in Mice.Function (Oxford, England) · 2025Article
- Important Aspects of siRNA Design for Optimal Efficacy In Vitro and In Vivo.International journal of cell biology · 2025Review
- Article
- Structure-activity relationship of amino acid analogs to probe the binding pocket of sodium-coupled neutral amino acid transporter SNAT2.Amino acids · 2024Article
- Trophoblast-specific overexpression of adiponectin receptor 2 causes fetal growth restriction in pregnant mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- Dietary Supplementation with 25-Hydroxyvitamin DAntioxidants (Basel, Switzerland) · 2024Article
- Article
- Regulation of placental amino acid transport in health and disease.Acta physiologica (Oxford, England) · 2024Review
- Trophoblast-specific overexpression of the LAT1 increases transplacental transport of essential amino acids and fetal growth in mice.PNAS nexus · 2024Article
- SNAT2-mediated regulation of estrogen and progesterone in the proliferation of goat mammary epithelial cells.Amino acids · 2024Article
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
Abstract
Fetal growth restriction (FGR) is a complication of pregnancy that reduces birth weight, markedly increases infant mortality and morbidity and is associated with later-life cardiometabolic disease. No specific treatment is available for FGR. Placentas of human FGR infants have low abundance of sodium-coupled neutral amino acid transporter 2 (Slc38a2/SNAT2), which supplies the fetus with amino acids required for growth. We determined the mechanistic role of placental Slc38a2/SNAT2 deficiency in the development of restricted fetal growth, hypothesizing that placenta-specific Slc38a2 knockdown causes FGR in mice. Using lentiviral transduction of blastocysts with a small hairpin RNA (shRNA), we achieved 59% knockdown of placental Slc38a2, without altering fetal Slc38a2 expression. Placenta-specific Slc38a2 knockdown reduced near-term fetal and placental weight, fetal viability, trophoblast plasma membrane (TPM) SNAT2 protein abundance, and both absolute and weight-specific placental uptake of the amino acid transport System A tracer, 14C-methylaminoisobutyric acid (MeAIB). We also measured human placental SLC38A2 gene expression in a well-defined term clinical cohort and found that SLC38A2 expression was decreased in late-onset, but not early-onset FGR, compared with appropriate for gestational age (AGA) control placentas. The results demonstrate that low placental Slc38a2/SNAT2 causes FGR and could be a target for clinical therapies for late-onset FGR.
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Registered trials
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.