Idiopathic pregnancy complications pose a major threat to both maternal and fetal health worldwide. Numerous studies have implicated the role of the renin-angiotensin system (RAS) in the development of obstetric syndromes, since it is crucial for the uteroplacental function. A major RAS component is the angiotensin-converting enzyme (ACE), which hydrolyses angiotensin I to angiotensin II, and not only regulates arterial pressure, but also fibrinolytic activity, indirectly, through the expression of plasminogen activator inhibitor-1. A key functional polymorphism of the ACE gene is the insertion/deletion (I/D) polymorphism, which affects gene expression and product levels, and can therefore lead to high blood pressure and/or reduced fibrinolytic activity. These can cause major pregnancy complications, such as preeclampsia, recurrent pregnancy loss and preterm birth. This review discusses how the ACE I/D is associated with susceptibility towards pregnancy complications, on its own or in combination with other functional gene polymorphisms such, as the angiotensin II receptor type 1 (AT1R) A1166CC, angiotensin II receptor type 2 (AT2R) G1332A, plasminogen activator inhibitor-1 (PAI-1) 4G/5G, matrix metallopeptidase-9 (MMP-9) C1562T, angiotensinogen (AGT) M235T, renin (REN) 83A/G, factor XIII (F13) Val34Leu and endothelial nitric oxide synthase (eNOS) 4a/b.

中文翻译：

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血管紧张素转换酶插入/缺失多态性作为主要妊娠并发症的常见危险因素

特发性妊娠并发症对全世界的孕产妇和胎儿健康构成重大威胁。许多研究表明肾素-血管紧张素系统 (RAS) 在产科综合征发展中的作用，因为它对子宫胎盘功能至关重要。RAS 的一个主要成分是血管紧张素转化酶 (ACE)，它将血管紧张素 I 水解为血管紧张素 II，不仅调节动脉压，而且还通过纤溶酶原激活剂抑制剂-1 的表达间接调节纤溶活性。ACE 基因的一个关键功能多态性是插入/缺失 (I/D) 多态性，它影响基因表达和产物水平，因此可导致高血压和/或纤溶活性降低。这些会导致严重的妊娠并发症，例如先兆子痫，反复流产和早产。本综述讨论了 ACE I/D 如何单独或与其他功能基因多态性（如血管紧张素 II 受体 1 型（AT1R）A1166CC、血管紧张素 II 受体 2 型（AT2R））与妊娠并发症的易感性相关联G1332A、纤溶酶原激活剂抑制剂-1 (PAI-1) 4G/5G、基质金属肽酶-9 (MMP-9) C1562T、血管紧张素原 (AGT) M235T、肾素 (REN) 83A/G、因子 XIII (F13) Val34Leu 和内皮硝酸盐氧化物合酶 (eNOS) 4a/b。