Konečná Barbora, Vlková Barbora, Celec Peter
Institute of Molecular Biomedicine, Faculty of Medicine, Comenius University, Bratislava, Slovakia.
Int J Mol Med. 2015 Feb;35(2):299-304. doi: 10.3892/ijmm.2014.2039. Epub 2014 Dec 15.
Preeclampsia is an autoimmune disorder characterized by hypertension. It begins with abnormal cytotrophoblast apoptosis, which leads to inflammation and an increase in the levels of anti-angiogenic factors followed by the disruption of the angiogenic status. Increased levels of fetal DNA and RNA coming from the placenta, one of the most commonly affected organs in pregnancies complicated by preeclampsia, have been found in pregnant women with the condition. However, it remains unknown as to whether this is a cause or a consequence of preeclampsia. Few studies have been carried out on preeclampsia in which an animal model of preeclampsia was induced by an injection of different types of DNA that are mimic fetal DNA and provoke inflammation through Toll-like receptor 9 (TLR9) or cyclic guanosine monophosphate-adenosine monophosphate (cGAMP). The specific mechanisms involved in the development of preeclampsia are not yet fully understood. It is hypothesized that the presence of different fragments of fetal DNA in maternal plasma may cause for the development of preeclampsia. The function of DNase during preeclampsia also remains unresolved. Studies have suggested that its activity is decreased or the DNA is protected against its effects. Further research is required to uncover the pathogenesis of preeclampsia and focus more on the condition of patients with the condition.
子痫前期是一种以高血压为特征的自身免疫性疾病。它始于细胞滋养层细胞异常凋亡，进而导致炎症以及抗血管生成因子水平升高，随后血管生成状态被破坏。在患有子痫前期的孕妇中，已发现来自胎盘（子痫前期妊娠中最常受影响的器官之一）的胎儿DNA和RNA水平升高。然而，这是子痫前期的原因还是结果仍不清楚。关于子痫前期，很少有研究通过注射模拟胎儿DNA并通过Toll样受体9（TLR9）或环磷酸鸟苷-磷酸腺苷（cGAMP）引发炎症的不同类型DNA来诱导子痫前期动物模型。子痫前期发展所涉及的具体机制尚未完全了解。据推测，母体血浆中存在不同片段的胎儿DNA可能导致子痫前期的发生。子痫前期期间脱氧核糖核酸酶的功能也仍未解决。研究表明其活性降低或DNA受到保护免受其影响。需要进一步研究以揭示子痫前期的发病机制，并更多地关注患有该疾病的患者的病情。
