Current State of Preeclampsia Mouse Models: Approaches, Relevance, and Standardization.
Current State of Preeclampsia Mouse Models: Approaches, Relevance, and Standardization.
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DOI：
10.3389/fphys.2021.681632
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发表时间：
2021
影响因子：
4
通讯作者：
Brown TL
中科院分区：
文献类型：
--
作者：
Waker CA;Kaufman MR;Brown TL
先兆子痫（PE）是一种多系统的，妊娠特异性疾病和孕产妇和胎儿死亡的主要原因。PE还与母亲和后代日后患慢性病的风险增加有关。胎盘形成或胎盘功能异常已被公认为PE发生的中心因素，但仍有许多关于这种情况的发展所涉及的因素有待确定。尽管经过数十年的研究和许多临床试验，唯一确定的治疗方法是分娩。为了更好地了解病情并在临床前鉴定潜在靶点，已经开发了许多模拟小鼠PE的方法，包括混合小鼠品系杂交、基因过表达和敲除、外源性药物给药、手术操作、全身性腺病毒感染和滋养层特异性基因转移。这些模型已被用于研究如何在人类PE中确定的生物扰动参与PE样症状的产生，并提高了对人类疾病的分子机制的理解。然而，这些方法的特征在于各种各样的生理终点，这可能使得难以比较模型之间的效果，并且这些方法中的许多方法具有与这种人类疾病缺乏生理相关性的方面，并且可能干扰治疗开发。这份报告提供了一个全面的审查小鼠模型，表现出PE样症状，并提出了标准化的生理特征分析小鼠模型的PE。
Preeclampsia (PE) is a multisystemic, pregnancy-specific disorder and a leading cause of maternal and fetal death. PE is also associated with an increased risk for chronic morbidities later in life for mother and offspring. Abnormal placentation or placental function has been well-established as central to the genesis of PE; yet much remains to be determined about the factors involved in the development of this condition. Despite decades of investigation and many clinical trials, the only definitive treatment is parturition. To better understand the condition and identify potential targets preclinically, many approaches to simulate PE in mice have been developed and include mixed mouse strain crosses, genetic overexpression and knockout, exogenous agent administration, surgical manipulation, systemic adenoviral infection, and trophoblast-specific gene transfer. These models have been useful to investigate how biological perturbations identified in human PE are involved in the generation of PE-like symptoms and have improved the understanding of the molecular mechanisms underpinning the human condition. However, these approaches were characterized by a wide variety of physiological endpoints, which can make it difficult to compare effects across models and many of these approaches have aspects that lack physiological relevance to this human disorder and may interfere with therapeutic development. This report provides a comprehensive review of mouse models that exhibit PE-like symptoms and a proposed standardization of physiological characteristics for analysis in murine models of PE.
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