Yongdan Ma , Yongyan Hu , Jiajun He , Xin Wen , Huixia Yang , Jingmei Ma
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引用次数: 0
Abstract
Introduction
Placenta accreta spectrum (PAS) is a serious condition associated with severe postpartum hemorrhage, leading to emergency hysterectomy. Research has predominantly focused on clinical diagnosis and the prevention of adverse maternal outcomes, but the underlying pathological mechanisms remain poorly understood, partly due to the limitations of animal models.
Methods
In this study, we conducted up to three cesarean sections (CS) on full-term pregnant mice, since a history of multiple CS is an independent risk factor for PAS. We evaluated pregnancy outcomes, placental development, morphology, trophoblast invasion, and angiogenesis at the maternal-fetal interface to assess the impact of repeated CS.
Results
Following repeated CS, the model mice displayed adverse pregnancy outcomes, including placental dysplasia, incomplete remodeling of spiral arteries, deep trophoblast invasion at the maternal-fetal interface, and reduced placental perfusion. Additionally, the mice exhibited abnormal fetal development, imbalances in angiogenic and anti-angiogenic both within the placenta and in peripheral blood.
Conclusion
The pathological phenotypes of placenta and adverse pregnancy outcomes observed in mice with a history of three CSs closely resemble the clinical features of PAS. This model offers a valuable tool for studying the pathogenesis of PAS and could serve as a foundation for the development of early prevention strategies.
导言胎盘早剥(PAS)是一种与严重产后出血相关的严重疾病,可导致紧急子宫切除术。本研究对足月妊娠小鼠进行了最多三次剖宫产手术(CS),因为多次剖宫产史是 PAS 的一个独立风险因素。结果重复剖宫产后,模型小鼠表现出不良的妊娠结局,包括胎盘发育不良、螺旋动脉重塑不完全、母胎界面滋养细胞深层侵入和胎盘灌注减少。此外,小鼠还表现出胎儿发育异常、胎盘内和外周血中血管生成和抗血管生成失衡。该模型为研究 PAS 的发病机制提供了宝贵的工具,并可作为开发早期预防策略的基础。
期刊介绍:
Placenta publishes high-quality original articles and invited topical reviews on all aspects of human and animal placentation, and the interactions between the mother, the placenta and fetal development. Topics covered include evolution, development, genetics and epigenetics, stem cells, metabolism, transport, immunology, pathology, pharmacology, cell and molecular biology, and developmental programming. The Editors welcome studies on implantation and the endometrium, comparative placentation, the uterine and umbilical circulations, the relationship between fetal and placental development, clinical aspects of altered placental development or function, the placental membranes, the influence of paternal factors on placental development or function, and the assessment of biomarkers of placental disorders.