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Sex differences in prenatal epigenetic programming of stress pathways.

机译:产前表观遗传编程的压力途径中的性别差异。

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摘要

Maternal stress experience is associated with neurodevelopmental disorders including schizophrenia and autism. Recent studies have examined mechanisms by which changes in the maternal milieu may be transmitted to the developing embryo and potentially translated into programming of the epigenome. Animal models of prenatal stress have identified important sex- and temporal-specific effects on offspring stress responsivity. As dysregulation of stress pathways is a common feature in most neuropsychiatric diseases, molecular and epigenetic analyses at the maternal-embryo interface, especially in the placenta, may provide unique insight into identifying much-needed predictive biomarkers. In addition, as most neurodevelopmental disorders present with a sex bias, examination of sex differences in the inheritance of phenotypic outcomes may pinpoint gene targets and specific windows of vulnerability in neurodevelopment, which have been disrupted. This review discusses the association and possible contributing mechanisms of prenatal stress in programming offspring stress pathway dysregulation and the importance of sex.
机译:产妇的压力经历与包括精神分裂症和自闭症在内的神经发育障碍有关。最近的研究已经检查了母体环境变化可以传递给发育中的胚胎并可能转化为表观基因组程序的机制。产前应激的动物模型已经确定了对后代应激反应性的重要性别和时间特异性影响。由于压力通路的失调是大多数神经精神疾病的常见特征,因此在母体-胚胎界面(尤其是在胎盘中)的分子和表观遗传学分析可以为识别急需的预测性生物标志物提供独特的见解。此外,由于大多数神经发育障碍都存在性别偏见,因此对表型结局遗传中的性别差异进行检查可能会查明已破坏的基因靶点和神经发育中特定的脆弱性窗口。这篇综述讨论了在编程后代应激途径失调和性的重要性方面,产前应激的关联和可能的作用机制。

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