Kanasaki Keizo, Kalluri Raghu
Department of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center, Boston, Massachusetts 02215, USA.
Kidney Int. 2009 Oct;76(8):831-7. doi: 10.1038/ki.2009.284. Epub 2009 Aug 5.
Preeclampsia is a systemic disease that results from placental defects and occurs in about 5-8% of pregnancies worldwide. Preeclampsia is a disease of many theories, wherein investigators put forward their favorite mechanistic ideas, each with a causal appeal for the pathogenesis of preeclampsia. In reality, the patho-mechanism of preeclampsia remains largely unknown. Preeclampsia, as diagnosed in patients today, is likely a heterogeneous collection of disease entities that share some common features but also show important differences. Therefore, one single mechanism may never be found to explain all the variants of preeclampsia. Current research must focus on evaluating such diverse mechanisms, as well as the possible common effector pathways. Here, we provide a discussion of several possible mechanisms and putative theories proposed for preeclampsia, with particular emphasis on the recent discovery of a new genetic mouse model offering new opportunities to explore experimental therapies.
子痫前期是一种由胎盘缺陷引起的全身性疾病,全球约5-8%的妊娠会发生该病。子痫前期是一种有多种理论的疾病,研究者们提出了各自中意的机制观点,每种观点都对子痫前期的发病机制有因果吸引力。实际上,子痫前期的发病机制在很大程度上仍不为人知。如今在患者中诊断出的子痫前期,可能是一组异质性疾病实体的集合,它们有一些共同特征,但也存在重要差异。因此,可能永远找不到单一机制来解释子痫前期的所有变体。当前的研究必须专注于评估如此多样的机制以及可能的共同效应途径。在此,我们讨论了为子痫前期提出的几种可能机制和假定理论,特别强调了最近发现的一种新的基因小鼠模型,它为探索实验性疗法提供了新机会。