Fetal Growth Regulation in Placental Development
Summary
The placenta is a multifunctional organ that governs fetal growth through the coordinated exchange of oxygen, nutrients and waste products, alongside the secretion of hormones and growth factors. Critical processes include invasion of maternal decidua by trophoblast cells, remodelling of uterine spiral arteries, and the establishment of a rich vascular network within the villous tree. Signalling pathways such as PI3K–Akt, mTOR and Wnt integrate maternal and fetal cues to adjust nutrient transporters and angiogenic factors. Epigenetic mechanisms, including DNA methylation and noncoding RNAs, fine-tune gene expression in trophoblast lineages, while imprinted genes regulate the balance between fetal demands and maternal resource allocation. Dysregulation of any of these components underlies intrauterine growth restriction (IUGR), which affects up to 10% of pregnancies globally, elevating the risk of perinatal morbidity and long-term metabolic and cardiovascular disease. Recent advances have begun to reveal how proteomic shifts, microRNAs and long noncoding RNAs converge on pathways of angiogenesis, cellular proliferation and invasion, offering new targets for early diagnosis and therapeutic intervention.
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Fetal Growth Regulation in Placental Development publication trend
The graph below shows the total number of articles in fetal growth regulation in placental development across all publications each year (not limited to Nature Index journals).
Technical terms
Trophoblast: specialised placental cell type responsible for implantation, modulation of maternal blood flow and nutrient transport.
Angiogenesis: formation of new blood vessels from existing vasculature, essential for nutrient and gas exchange in the placenta.
Intrauterine growth restriction (IUGR): pathological condition in which a fetus fails to achieve its genetically predetermined growth potential, often due to placental insufficiency.
Long noncoding RNA (lncRNA): RNA transcripts longer than 200 nucleotides that do not code for protein but regulate gene expression at transcriptional and post-transcriptional levels.
MicroRNA (miRNA): small (~22 nucleotides) noncoding RNA molecules that bind target mRNAs to repress translation or promote degradation, fine-tuning protein output.
References
- The Proteome Landscape of Human Placentas for Monochorionic Twins with Selective Intrauterine Growth Restriction. Genomics Proteomics & Bioinformatics (2023).
- The Role of MALAT1 in Regulating the Proangiogenic Functions, Invasion, and Migration of Trophoblasts in Selective Fetal Growth Restriction. Biomolecules (2024).
- An miRNA-mRNA integrative analysis in human placentas and mice: role of the Smad2/miR-155-5p axis in the development of fetal growth restriction. Frontiers in Bioengineering and Biotechnology (2023).
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