Sosnowski David W, Booth Carolyn, York Timothy P, Amstadter Ananda B, Kliewer Wendy
Department of Psychology, Virginia Commonwealth University, Richmond, Virginia.
Department of Human and Molecular Genetics, Virginia Commonwealth University, Richmond, Virginia.
Dev Psychobiol. 2018 Mar;60(2):127-139. doi: 10.1002/dev.21604. Epub 2018 Jan 18.
Maternal prenatal stress has been linked to a variety of infant postnatal outcomes, partially through alterations in fetal HPA axis functioning; yet the underlying pathobiology remains elusive. Current literature posits DNA methylation as a candidate mechanism through which maternal prenatal stress can influence fetal HPA axis functioning. The goal of this systematic review was to summarize the literature examining the associations among maternal prenatal stress, DNA methylation of commonly studied HPA axis candidate genes, and infant HPA axis functioning. Results from the review provided evidence for a link between various maternal prenatal stressors, NR3C1 methylation, and infant stress reactivity, but findings among other genes were limited, with mixed results. An original study quality review tool revealed that a majority of studies in the review are adequate, and emphasizes the need for future research to consider study quality when interpreting research findings.
母亲产前应激与多种婴儿产后结局有关,部分原因是通过胎儿下丘脑-垂体-肾上腺(HPA)轴功能的改变;然而,潜在的病理生物学机制仍然难以捉摸。当前文献认为DNA甲基化是母亲产前应激可能影响胎儿HPA轴功能的一种候选机制。本系统综述的目的是总结研究母亲产前应激、常用的HPA轴候选基因的DNA甲基化和婴儿HPA轴功能之间关联的文献。综述结果为各种母亲产前应激源、NR3C1甲基化和婴儿应激反应性之间的联系提供了证据,但其他基因的研究结果有限,且结果不一。一项原创的研究质量审查工具显示,该综述中的大多数研究是充分的,并强调未来研究在解释研究结果时需要考虑研究质量。