Department of Obstetrics and Gynecology, Division of Maternal-Fetal Medicine, The University of Texas Medical Branch at Galveston, TX 77555, USA.
Reprod Sci. 2012 Jan;19(1):6-13. doi: 10.1177/1933719111424446.
Spontaneous preterm birth (PTB; birth prior to 37 weeks of gestation) is a complex phenotype with multiple risk factors that complicate our understanding of its etiology. A number of recent studies have supported the hypothesis that epigenetic modifications such as DNA methylation induced by pregnancy-related risk factors may influence the risk of PTB or result in changes that predispose a neonate to adult-onset diseases. The critical role of timing of gene expression in the etiology of PTB makes it a highly relevant disorder in which to examine the potential role of epigenetic changes. Because changes in DNA methylation patterns can result in long-term consequences, it is of critical interest to identify the epigenetic patterns associated with adverse pregnancy outcomes. This review examines the potential role of DNA methylation as a risk factor for PTB and discusses several issues and limitations that should be considered when planning DNA methylation studies.
自发性早产(PTB;妊娠 37 周前分娩)是一种具有多种风险因素的复杂表型,这使得我们难以理解其病因。最近的许多研究支持了这样一种假设,即妊娠相关风险因素诱导的表观遗传修饰(如 DNA 甲基化)可能会影响 PTB 的风险,或导致新生儿易患成人疾病的变化。基因表达时间在 PTB 病因中的关键作用使其成为一个高度相关的疾病,在该疾病中可以检验表观遗传变化的潜在作用。由于 DNA 甲基化模式的变化可能会导致长期后果,因此确定与不良妊娠结局相关的表观遗传模式至关重要。这篇综述探讨了 DNA 甲基化作为 PTB 风险因素的潜在作用,并讨论了在规划 DNA 甲基化研究时应考虑的几个问题和局限性。