Animal models of the placenta accreta spectrum: current status and further perspectives

Placenta accreta spectrum disorder (PAS) is a kind of disease of placentation defined as abnormal trophoblast invasion of part or all of the placenta into the myometrium, even penetrating the uterus. Decidual deficiency, abnormal vascular remodeling in the maternal–fetal interface, and excessive inv...

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Main Authors: Yongdan Ma, Yongyan Hu, Jingmei Ma
Format: Article
Language:English
Published: Frontiers Media S.A. 2023-05-01
Series:Frontiers in Endocrinology
Subjects:
Online Access:https://www.frontiersin.org/articles/10.3389/fendo.2023.1118168/full
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author Yongdan Ma
Yongyan Hu
Jingmei Ma
Jingmei Ma
author_facet Yongdan Ma
Yongyan Hu
Jingmei Ma
Jingmei Ma
author_sort Yongdan Ma
collection DOAJ
description Placenta accreta spectrum disorder (PAS) is a kind of disease of placentation defined as abnormal trophoblast invasion of part or all of the placenta into the myometrium, even penetrating the uterus. Decidual deficiency, abnormal vascular remodeling in the maternal–fetal interface, and excessive invasion by extravillous trophoblast (EVT) cells contribute to its onset. However, the mechanisms and signaling pathways underlying such phenotypes are not fully understood, partly due to the lack of suitable experimental animal models. Appropriate animal models will facilitate the comprehensive and systematic elucidation of the pathogenesis of PAS. Due to the remarkably similar functional placental villous units and hemochorial placentation to humans, the current animal models of PAS are based on mice. There are various mouse models induced by uterine surgery to simulate different phenotypes of PAS, such as excessive invasion of EVT or immune disturbance at the maternal–fetal interface, which could define the pathological mechanism of PAS from the perspective of the “soil.” Additionally, genetically modified mouse models could be used to study PAS, which is helpful to exploring the pathogenesis of PAS from the perspectives of both “soil” and “seed,” respectively. This review details early placental development in mice, with a focus on the approaches of PAS modeling. Additionally, the strengths, limitations and the applicability of each strategy and further perspectives are summarized to provide the theoretical foundation for researchers to select appropriate animal models for various research purposes. This will help better determine the pathogenesis of PAS and even promote possible therapy.
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spelling doaj.art-5ba8662d5e7f4f0181a973d95087a3c32023-05-08T04:58:49ZengFrontiers Media S.A.Frontiers in Endocrinology1664-23922023-05-011410.3389/fendo.2023.11181681118168Animal models of the placenta accreta spectrum: current status and further perspectivesYongdan Ma0Yongyan Hu1Jingmei Ma2Jingmei Ma3Department of Obstetrics and Gynecology, Peking University First Hospital, Beijing, ChinaLaboratory Animal Center, Peking University First Hospital, Beijing, ChinaDepartment of Obstetrics and Gynecology, Peking University First Hospital, Beijing, ChinaBeijing Key Laboratory of Maternal Fetal Medicine of Gestational Diabetes Mellitus, Beijing, ChinaPlacenta accreta spectrum disorder (PAS) is a kind of disease of placentation defined as abnormal trophoblast invasion of part or all of the placenta into the myometrium, even penetrating the uterus. Decidual deficiency, abnormal vascular remodeling in the maternal–fetal interface, and excessive invasion by extravillous trophoblast (EVT) cells contribute to its onset. However, the mechanisms and signaling pathways underlying such phenotypes are not fully understood, partly due to the lack of suitable experimental animal models. Appropriate animal models will facilitate the comprehensive and systematic elucidation of the pathogenesis of PAS. Due to the remarkably similar functional placental villous units and hemochorial placentation to humans, the current animal models of PAS are based on mice. There are various mouse models induced by uterine surgery to simulate different phenotypes of PAS, such as excessive invasion of EVT or immune disturbance at the maternal–fetal interface, which could define the pathological mechanism of PAS from the perspective of the “soil.” Additionally, genetically modified mouse models could be used to study PAS, which is helpful to exploring the pathogenesis of PAS from the perspectives of both “soil” and “seed,” respectively. This review details early placental development in mice, with a focus on the approaches of PAS modeling. Additionally, the strengths, limitations and the applicability of each strategy and further perspectives are summarized to provide the theoretical foundation for researchers to select appropriate animal models for various research purposes. This will help better determine the pathogenesis of PAS and even promote possible therapy.https://www.frontiersin.org/articles/10.3389/fendo.2023.1118168/fullplacenta accreta spectrumanimal modelplacenta developmentmouse placentatrophoblast invasiondecidual deficiency
spellingShingle Yongdan Ma
Yongyan Hu
Jingmei Ma
Jingmei Ma
Animal models of the placenta accreta spectrum: current status and further perspectives
Frontiers in Endocrinology
placenta accreta spectrum
animal model
placenta development
mouse placenta
trophoblast invasion
decidual deficiency
title Animal models of the placenta accreta spectrum: current status and further perspectives
title_full Animal models of the placenta accreta spectrum: current status and further perspectives
title_fullStr Animal models of the placenta accreta spectrum: current status and further perspectives
title_full_unstemmed Animal models of the placenta accreta spectrum: current status and further perspectives
title_short Animal models of the placenta accreta spectrum: current status and further perspectives
title_sort animal models of the placenta accreta spectrum current status and further perspectives
topic placenta accreta spectrum
animal model
placenta development
mouse placenta
trophoblast invasion
decidual deficiency
url https://www.frontiersin.org/articles/10.3389/fendo.2023.1118168/full
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