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Regulators involved in trophoblast syncytialization in the placenta of intrauterine growth restriction

Placental dysfunction refers to the insufficiency of placental perfusion and chronic hypoxia during early pregnancy, which impairs placental function and causes inadequate supply of oxygen and nutrients to the fetus, affecting fetal development and health. Fetal intrauterine growth restriction, one...

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Autores principales: Zhou, Hanjing, Zhao, Chenqiong, Wang, Peixin, Yang, Weijie, Zhu, Haiyan, Zhang, Songying
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9927020/
https://www.ncbi.nlm.nih.gov/pubmed/36798658
http://dx.doi.org/10.3389/fendo.2023.1107182
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author Zhou, Hanjing
Zhao, Chenqiong
Wang, Peixin
Yang, Weijie
Zhu, Haiyan
Zhang, Songying
author_facet Zhou, Hanjing
Zhao, Chenqiong
Wang, Peixin
Yang, Weijie
Zhu, Haiyan
Zhang, Songying
author_sort Zhou, Hanjing
collection PubMed
description Placental dysfunction refers to the insufficiency of placental perfusion and chronic hypoxia during early pregnancy, which impairs placental function and causes inadequate supply of oxygen and nutrients to the fetus, affecting fetal development and health. Fetal intrauterine growth restriction, one of the most common outcomes of pregnancy-induced hypertensions, can be caused by placental dysfunction, resulting from deficient trophoblast syncytialization, inadequate trophoblast invasion and impaired vascular remodeling. During placental development, cytotrophoblasts fuse to form a multinucleated syncytia barrier, which supplies oxygen and nutrients to meet the metabolic demands for fetal growth. A reduction in the cell fusion index and the number of nuclei in the syncytiotrophoblast are found in the placentas of pregnancies complicated by IUGR, suggesting that the occurrence of IUGR may be related to inadequate trophoblast syncytialization. During the multiple processes of trophoblasts syncytialization, specific proteins and several signaling pathways are involved in coordinating these events and regulating placental function. In addition, epigenetic modifications, cell metabolism, senescence, and autophagy are also involved. Study findings have indicated several abnormally expressed syncytialization-related proteins and signaling pathways in the placentas of pregnancies complicated by IUGR, suggesting that these elements may play a crucial role in the occurrence of IUGR. In this review, we discuss the regulators of trophoblast syncytialization and their abnormal expression in the placentas of pregnancies complicated by IUGR.
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spelling pubmed-99270202023-02-15 Regulators involved in trophoblast syncytialization in the placenta of intrauterine growth restriction Zhou, Hanjing Zhao, Chenqiong Wang, Peixin Yang, Weijie Zhu, Haiyan Zhang, Songying Front Endocrinol (Lausanne) Endocrinology Placental dysfunction refers to the insufficiency of placental perfusion and chronic hypoxia during early pregnancy, which impairs placental function and causes inadequate supply of oxygen and nutrients to the fetus, affecting fetal development and health. Fetal intrauterine growth restriction, one of the most common outcomes of pregnancy-induced hypertensions, can be caused by placental dysfunction, resulting from deficient trophoblast syncytialization, inadequate trophoblast invasion and impaired vascular remodeling. During placental development, cytotrophoblasts fuse to form a multinucleated syncytia barrier, which supplies oxygen and nutrients to meet the metabolic demands for fetal growth. A reduction in the cell fusion index and the number of nuclei in the syncytiotrophoblast are found in the placentas of pregnancies complicated by IUGR, suggesting that the occurrence of IUGR may be related to inadequate trophoblast syncytialization. During the multiple processes of trophoblasts syncytialization, specific proteins and several signaling pathways are involved in coordinating these events and regulating placental function. In addition, epigenetic modifications, cell metabolism, senescence, and autophagy are also involved. Study findings have indicated several abnormally expressed syncytialization-related proteins and signaling pathways in the placentas of pregnancies complicated by IUGR, suggesting that these elements may play a crucial role in the occurrence of IUGR. In this review, we discuss the regulators of trophoblast syncytialization and their abnormal expression in the placentas of pregnancies complicated by IUGR. Frontiers Media S.A. 2023-01-31 /pmc/articles/PMC9927020/ /pubmed/36798658 http://dx.doi.org/10.3389/fendo.2023.1107182 Text en Copyright © 2023 Zhou, Zhao, Wang, Yang, Zhu and Zhang https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Endocrinology
Zhou, Hanjing
Zhao, Chenqiong
Wang, Peixin
Yang, Weijie
Zhu, Haiyan
Zhang, Songying
Regulators involved in trophoblast syncytialization in the placenta of intrauterine growth restriction
title Regulators involved in trophoblast syncytialization in the placenta of intrauterine growth restriction
title_full Regulators involved in trophoblast syncytialization in the placenta of intrauterine growth restriction
title_fullStr Regulators involved in trophoblast syncytialization in the placenta of intrauterine growth restriction
title_full_unstemmed Regulators involved in trophoblast syncytialization in the placenta of intrauterine growth restriction
title_short Regulators involved in trophoblast syncytialization in the placenta of intrauterine growth restriction
title_sort regulators involved in trophoblast syncytialization in the placenta of intrauterine growth restriction
topic Endocrinology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9927020/
https://www.ncbi.nlm.nih.gov/pubmed/36798658
http://dx.doi.org/10.3389/fendo.2023.1107182
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