Neurodevelopmental consequences in offspring of mothers with preeclampsia during pregnancy: underlying biological mechanism via imprinting genes.
Neurodevelopmental consequences in offspring of mothers with preeclampsia during pregnancy: underlying biological mechanism via imprinting genes.
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DOI：
10.1007/s00404-017-4347-3
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发表时间：
2017-06
影响因子：
2.6
通讯作者：
Lambertini L
中科院分区：
文献类型：
--
作者：
Nomura Y;John RM;Janssen AB;Davey C;Finik J;Buthmann J;Glover V;Lambertini L
先兆子痫是已知的母亲和她们的婴儿的死亡率和发病率的主要原因。在美国，大约3-8%的妊娠合并先兆子痫，另外5-7%合并高血压症状。然而，很少有人知道它对婴儿神经行为发育的长期影响。目前的审查试图证明高血压引起的印迹基因失调的新证据，这可能解释母亲先兆子痫和后代神经认知失调之间的联系。使用术语“先兆子痫”、“妊娠期高血压”、“印记基因”、“印记失调”和“表观遗传修饰”检索PubMed和Web of Science数据库，以回顾表明先兆子痫和次优儿童神经发育之间相关性的证据，并表明胎盘基因组印记失调是潜在的潜在机制。众所周知，先兆子痫导致母亲和胎儿的死亡率和发病率很高，但关于先兆子痫的长期生物学后果以及由此产生的缺氧对胎儿/儿童神经发育的影响的研究很少。在过去的十年中，来自超越学科界限的研究的越来越多的证据已经开始表明，胎盘中表达的印记基因可能为先兆子痫和认知神经发育受损之间的联系提供线索。胎盘检测到的孕产妇高血压突然发作可能会通过表观基因组的变化导致胎儿的生物编程被误导，从而导致婴儿发育不佳。进一步了解胎儿/婴儿神经发育轨迹受先兆子痫和高血压影响的分子和细胞机制，将是预防婴儿不良神经发育的重要第一步。
Preeclampsia is known to be a leading cause of mortality and morbidity among mothers and their infants. Approximately 3–8% of all pregnancies in the US are complicated by preeclampsia and another 5–7% by hypertensive symptoms. However, less is known about its long-term influence on infant neurobehavioral development. The current review attempts to demonstrate new evidence for imprinting gene dysregulation caused by hypertension, which may explain the link between maternal preeclampsia and neurocognitive dysregulation in offspring. Pub Med and Web of Science databases were searched using the terms “preeclampsia,” “gestational hypertension,” “imprinting genes,” “imprinting dysregulation,” and “epigenetic modification,” in order to review the evidence demonstrating associations between preeclampsia and suboptimal child neurodevelopment, and suggest dysregulation of placental genomic imprinting as a potential underlying mechanism. The high mortality and morbidity among mothers and fetuses due to preeclampsia is well known, but there is little research on the long-term biological consequences of preeclampsia and resulting hypoxia on the fetal/child neurodevelopment. In the past decade, accumulating evidence from studies that transcend disciplinary boundaries have begun to show that imprinted genes expressed in the placenta might hold clues for a link between preeclampsia and impaired cognitive neurodevelopment. A sudden onset of maternal hypertension detected by the placenta may result in misguided biological programming of the fetus via changes in the epigenome, resulting in suboptimal infant development. Furthering our understanding of the molecular and cellular mechanisms through which neurodevelopmental trajectories of the fetus/infant are affected by preeclampsia and hypertension will represent an important first step toward preventing adverse neurodevelopment in infants.
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