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Placental adaptations supporting fetal growth during normal and adverse gestational environments.
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- Author(s): Sferruzzi-Perri AN;Sferruzzi-Perri AN; Lopez-Tello J; Lopez-Tello J; Salazar-Petres E; Salazar-Petres E; Salazar-Petres E
- Source:
Experimental physiology [Exp Physiol] 2023 Mar; Vol. 108 (3), pp. 371-397. Date of Electronic Publication: 2022 Dec 09.- Publication Type:
Journal Article; Review; Research Support, Non-U.S. Gov't- Language:
English - Source:
- Additional Information
- Source: Publisher: Wiley-Blackwell Country of Publication: England NLM ID: 9002940 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1469-445X (Electronic) Linking ISSN: 09580670 NLM ISO Abbreviation: Exp Physiol Subsets: MEDLINE
- Publication Information: Publication: Cambridge, Eng : Wiley-Blackwell
Original Publication: Cambridge ; New York, NY, USA : Published for the Physiological Society by Cambridge University Press, c1990- - Subject Terms:
- Abstract: New Findings: What is the topic of this review? How the placenta, which transports nutrients and oxygen to the fetus, may alter its support of fetal growth developmentally and with adverse gestational conditions. What advances does it highlight? Placental formation and function alter with the needs of the fetus for substrates for growth during normal gestation and when there is enhanced competition for substrates in species with multiple gestations or adverse gestational environments, and this is mediated by imprinted genes, signalling pathways, mitochondria and fetal sexomes.
Abstract: The placenta is vital for mammalian development and a key determinant of life-long health. It is the interface between the mother and fetus and is responsible for transporting the nutrients and oxygen a fetus needs to develop and grow. Alterations in placental formation and function, therefore, have consequences for fetal growth and birthweight, which in turn determine perinatal survival and risk of non-communicable diseases for the offspring in later postnatal life. However, the placenta is not a static organ. As this review summarizes, research from multiple species has demonstrated that placental formation and function alter developmentally to the needs of the fetus for substrates for growth during normal gestation, as well as when there is greater competition for substrates in polytocous species and monotocous species with multiple gestations. The placenta also adapts in response to the gestational environment, integrating information about the ability of the mother to provide nutrients and oxygen with the needs of the fetus in that prevailing environment. In particular, placental structure (e.g. vascularity, surface area, blood flow, diffusion distance) and transport capacity (e.g. nutrient transporter levels and activity) respond to suboptimal gestational environments, namely malnutrition, obesity, hypoxia and maternal ageing. Mechanisms mediating developmentally and environmentally induced homeostatic responses of the placenta that help support normal fetal growth include imprinted genes, signalling pathways, subcellular constituents and fetal sexomes. Identification of these placental strategies may inform the development of therapies for complicated human pregnancies and advance understanding of the pathways underlying poor fetal outcomes and their consequences for health and disease risk.
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Front Endocrinol (Lausanne). 2018 Nov 20;9:671. (PMID: 30515131) - Grant Information: United Kingdom WT_ Wellcome Trust; MR/R022690/1 United Kingdom MRC_ Medical Research Council; 220456/Z/20/Z United Kingdom WT_ Wellcome Trust; MR/R022690/1/RG93186 United Kingdom MRC_ Medical Research Council
- Contributed Indexing: Keywords: ageing; fetus; hypoxia; malnutrition; mitochondria; nutrient; obesity; placenta; pregnancy; sex differences
- Accession Number: 0 (Membrane Transport Proteins)
S88TT14065 (Oxygen) - Publication Date: Date Created: 20221209 Date Completed: 20230302 Latest Revision: 20240411
- Publication Date: 20240411
- Accession Number: PMC10103877
- Accession Number: 10.1113/EP090442
- Accession Number: 36484327
- Source:
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