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子痫前期:连接血管生成和代谢途径。

Pre-eclampsia: connecting angiogenic and metabolic pathways.

机构信息

Division of Matrix Biology, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA 02215, USA.

出版信息

Trends Endocrinol Metab. 2010 Sep;21(9):529-36. doi: 10.1016/j.tem.2010.05.002. Epub 2010 Jun 18.

Abstract

Pre-eclampsia is a hypertensive disease of pregnancy with a worldwide incidence of 5-8%. This review focuses on recent developments in pre-eclampsia research related to angiogenesis and metabolism. We first address the 'angiogenic imbalance' theory, which hypothesizes that pre-eclampsia results from an imbalance of factors that promote or antagonize angiogenesis, such as soluble fms-like tyrosine kinase (sFlt1), 2-methoxyestradiol (2-ME) and catechol-O-methyltransferase (COMT). Next, we analyze the association between pre-eclampsia and dysfunctional metabolism of both homocysteine and placental glycogen. We hope that illuminating some of the various connections existing between angiogenesis and metabolism in pre-eclampsia will facilitate the update or reconsideration of old models of pathogenesis.

摘要

子痫前期是一种妊娠高血压疾病,全球发病率为 5-8%。本综述重点介绍了与血管生成和代谢相关的子痫前期研究的最新进展。我们首先讨论了“血管生成失衡”理论,该理论假设子痫前期是由促进或拮抗血管生成的因素失衡引起的,如可溶性 fms 样酪氨酸激酶 (sFlt1)、2-甲氧基雌二醇 (2-ME) 和儿茶酚-O-甲基转移酶 (COMT)。接下来,我们分析了子痫前期与同型半胱氨酸和胎盘糖原代谢功能障碍之间的关系。我们希望阐明子痫前期中血管生成和代谢之间存在的一些不同联系,将有助于更新或重新考虑旧的发病机制模型。

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