Mütze Sabine, Rudnik-Schöneborn Sabine, Zerres Klaus, Rath Werner
Department of Obstetrics and Gynecology, Aachen University (RWTH), Aachen, Germany.
J Perinat Med. 2008;36(1):38-58. doi: 10.1515/JPM.2008.004.
Preeclampsia is specific to pregnancy and is still a leading cause of maternal and perinatal mortality and morbidity, affecting about 3% of women, but the underlying pathogenetic mechanisms still remain unclear. Immune maladaptation, placental ischemia and increased oxidative stress represent the main components discussed to be of etiologic importance, and they all may have genetic implications. Since the familial nature of preeclampsia is known for many years, extensive research on the genetic contribution to the pathogenesis of this severe pregnancy disorder has been performed. In this review, we will overview the linkage and candidate gene studies carried out so far as well as summarize important historical notes on the genetic hypotheses generated in preeclampsia research. Moreover, the influence of maternal and fetal genes and their interaction as well as the role of genomic imprinting in preeclampsia will be discussed.
子痫前期是妊娠期特有的疾病，仍是孕产妇和围产儿发病和死亡的主要原因，约3% 的孕妇受其影响，但其潜在的发病机制仍不清楚。免疫适应不良、胎盘缺血和氧化应激增加是讨论中具有病因学重要性的主要因素，它们都可能具有遗传学意义。由于子痫前期的家族性已为人所知多年，因此已经对这种严重妊娠疾病发病机制的遗传因素进行了广泛研究。在这篇综述中，我们将概述迄今为止进行的连锁和候选基因研究，并总结子痫前期研究中产生的遗传假说的重要历史记录。此外，还将讨论母体和胎儿基因的影响及其相互作用以及基因组印记在子痫前期中的作用。
