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

胎盘形成 胎盘植入 发病机制 滋养层 胎盘 生物 机制(生物学) 表型 动物模型 胎儿 生物信息学 怀孕 免疫学 遗传学 内分泌学 哲学 认识论 基因
作者
Yong-dan Ma,Yongyan Hu,Jingmei Ma
出处
期刊:Frontiers in Endocrinology [Frontiers Media]
卷期号:14: 1118168-1118168 被引量:15
标识
DOI:10.3389/fendo.2023.1118168
摘要

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.
最长约 10秒,即可获得该文献文件

科研通智能强力驱动
Strongly Powered by AbleSci AI
科研通是完全免费的文献互助平台,具备全网最快的应助速度,最高的求助完成率。 对每一个文献求助,科研通都将尽心尽力,给求助人一个满意的交代。
实时播报
NGU发布了新的文献求助10
1秒前
虚幻毛巾完成签到,获得积分20
1秒前
1秒前
懒羊羊大王完成签到,获得积分10
1秒前
sun完成签到,获得积分10
2秒前
aajhajkahna的应助被尘冀等待采纳,获得10
2秒前
2秒前
哈哈哈完成签到,获得积分10
2秒前
123发布了新的文献求助10
3秒前
ing完成签到 ,获得积分10
3秒前
诸葛明明的应助被科研通管家采纳,获得10
6秒前
李健的应助被科研通管家采纳,获得10
6秒前
sun发布了新的文献求助10
6秒前
852的应助被科研通管家采纳,获得10
6秒前
6秒前
wanci的应助被科研通管家采纳,获得10
7秒前
7秒前
ding的应助被科研通管家采纳,获得10
7秒前
你好你好的应助被科研通管家采纳,获得10
7秒前
极限001的应助被科研通管家采纳,获得10
7秒前
Lucas的应助被科研通管家采纳,获得10
7秒前
7秒前
7秒前
所所的应助被科研通管家采纳,获得10
7秒前
null的应助被科研通管家采纳,获得10
8秒前
8秒前
开朗的碧灵完成签到 ,获得积分10
9秒前
arran1111发布了新的文献求助10
9秒前
年轻千愁发布了新的文献求助10
9秒前
发阿发完成签到,获得积分10
10秒前
YH发布了新的文献求助10
12秒前
zgmhemtt发布了新的文献求助20
12秒前
成就茗完成签到,获得积分10
12秒前
13秒前
彭于晏的应助被头发永远茂盛采纳,获得10
15秒前
17秒前
回家睡觉完成签到,获得积分10
20秒前
20秒前
YH完成签到,获得积分10
21秒前
Bizi完成签到,获得积分10
22秒前
高分求助中
(应助此贴封号)通过应助OA文献获取积分 10000
Rosenblum, Global Change Biology 800
The Student's Guide to Social Neuroscience 600
Computational Chemical Reaction Engineering: Modeling, Simulation, and Design with MATLAB 600
Organizational Behavior 510
Management and the Arts 510
A Will for the Machine: Computerization, Automation, and the Arts in South Africa 400
热门求助领域 (近24小时)
化学 材料科学 医学 生物 计算机科学 工程类 纳米技术 内科学 物理 有机化学 化学工程 生物化学 复合材料 光电子学 细胞生物学 心理学 量子力学 催化作用 物理化学 电极
热门帖子
关注 科研通微信公众号,转发送积分 7810627
求助须知:如何正确求助?哪些是违规求助? 9342298
关于积分的说明 20512102
捐赠科研通 7403471
什么是DOI,文献DOI怎么找? 3329412
关于科研通互助平台的介绍 2476320
邀请新用户注册赠送积分活动 2348354