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患有合并症的子痫前期小鼠模型。

Mouse models of preeclampsia with preexisting comorbidities.

作者信息

Waker Christopher A, Hwang Amy E, Bowman-Gibson Scout, Chandiramani Chandni H, Linkous Bryce, Stone Madison L, Keoni Chanel I, Kaufman Melissa R, Brown Thomas L

机构信息

Department of Neuroscience, Cell Biology and Physiology, Boonshoft School of Medicine, Wright State University, Dayton, OH, United States.

Department of Obstetrics and Gynecology, Boonshoft School of Medicine, Wright State University, Dayton, OH, United States.

出版信息

Front Physiol. 2023 Apr 6;14:1137058. doi: 10.3389/fphys.2023.1137058. eCollection 2023.

DOI:10.3389/fphys.2023.1137058
PMID:37089425
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10117893/
Abstract

Preeclampsia is a pregnancy-specific condition and a leading cause of maternal and fetal morbidity and mortality. It is thought to occur due to abnormal placental development or dysfunction, because the only known cure is delivery of the placenta. Several clinical risk factors are associated with an increased incidence of preeclampsia including chronic hypertension, diabetes, autoimmune conditions, kidney disease, and obesity. How these comorbidities intersect with preeclamptic etiology, however, is not well understood. This may be due to the limited number of animal models as well as the paucity of studies investigating the impact of these comorbidities. This review examines the current mouse models of chronic hypertension, pregestational diabetes, and obesity that subsequently develop preeclampsia-like symptoms and discusses how closely these models recapitulate the human condition. Finally, we propose an avenue to expand the development of mouse models of preeclampsia superimposed on chronic comorbidities to provide a strong foundation needed for preclinical testing.

摘要

子痫前期是一种与妊娠相关的疾病,是孕产妇和胎儿发病及死亡的主要原因。其发病被认为是由于胎盘发育异常或功能障碍所致,因为目前已知的唯一治疗方法是娩出胎盘。子痫前期发病率增加与多种临床风险因素相关,包括慢性高血压、糖尿病、自身免疫性疾病、肾脏疾病和肥胖。然而,这些合并症如何与子痫前期的病因相互作用,目前尚不清楚。这可能是由于动物模型数量有限,以及研究这些合并症影响的研究较少。本综述探讨了目前随后会出现子痫前期样症状的慢性高血压、孕前糖尿病和肥胖的小鼠模型,并讨论了这些模型与人类疾病的相似程度。最后,我们提出了一条途径,以扩大子痫前期叠加慢性合并症小鼠模型的开发,为临床前试验提供坚实的基础。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d273/10117893/044351d266df/fphys-14-1137058-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d273/10117893/044351d266df/fphys-14-1137058-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d273/10117893/044351d266df/fphys-14-1137058-g001.jpg

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本文引用的文献

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Maternal and neonatal complications in women with medical comorbidities and preeclampsia.患有合并症的子痫前期妇女的母婴并发症。
Pregnancy Hypertens. 2022 Mar;27:62-68. doi: 10.1016/j.preghy.2021.12.006. Epub 2021 Dec 16.
2
Hypertension in Pregnancy: Diagnosis, Blood Pressure Goals, and Pharmacotherapy: A Scientific Statement From the American Heart Association.妊娠期高血压:诊断、血压目标和药物治疗:美国心脏协会科学声明。
Hypertension. 2022 Feb;79(2):e21-e41. doi: 10.1161/HYP.0000000000000208. Epub 2021 Dec 15.
3
The BPH/5 Mouse Model of Superimposed Preeclampsia Is Not a Model of HELLP Syndrome.
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Reprod Sci. 2024 Sep;31(9):2771-2782. doi: 10.1007/s43032-024-01591-y. Epub 2024 May 22.
4
Guidelines for assessing maternal cardiovascular physiology during pregnancy and postpartum.妊娠期及产褥期女性心血管生理学评估指南。
Am J Physiol Heart Circ Physiol. 2024 Jul 1;327(1):H191-H220. doi: 10.1152/ajpheart.00055.2024. Epub 2024 May 17.
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Involvement of metalloproteinase and nitric oxide synthase/nitric oxide mechanisms in early decidual angiogenesis-vascularization of normal and experimental pathological mouse placenta related to maternal alcohol exposure.金属蛋白酶和一氧化氮合酶/一氧化氮机制在正常及实验性病理小鼠胎盘早期蜕膜血管生成-血管化中的作用,该病理状态与母体酒精暴露有关。
Front Cell Dev Biol. 2023 Aug 16;11:1207671. doi: 10.3389/fcell.2023.1207671. eCollection 2023.
BPH/5 叠加子痫前期小鼠模型并非 HELLP 综合征模型。
Biology (Basel). 2021 Nov 14;10(11):1179. doi: 10.3390/biology10111179.
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Placenta-specific Slc38a2/SNAT2 knockdown causes fetal growth restriction in mice.胎盘特异性 Slc38a2/SNAT2 敲低导致小鼠胎儿生长受限。
Clin Sci (Lond). 2021 Sep 17;135(17):2049-2066. doi: 10.1042/CS20210575.
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Drug Discov Today. 2021 Nov;26(11):2754-2773. doi: 10.1016/j.drudis.2021.07.011. Epub 2021 Jul 22.
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Front Physiol. 2021 Jul 2;12:681632. doi: 10.3389/fphys.2021.681632. eCollection 2021.
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