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子痫前期发病机制至今尚未完全阐明。目前认为子痫前期的发病源于胎盘病理生理改变,进一步导致全身血管内皮细胞损伤,进而引起子痫前期的一系列临床症状。血管内皮细胞损伤是子痫前期病因学的中心环节,其中氧化与抗氧化失衡,血管活性因子异常分泌,凝血功能异常以及基因的多态性或异常表达等都对血管内皮细胞损伤起重要作用。现就这些变化与内皮细胞损伤的关系作一综述,探讨其在子痫前期发病中的作用。
The pathogenesis of preeclampsia has not yet been fully elucidated. It is currently believed that the pathogenesis of preeclampsia is due to pathophysiological changes in the placenta, further leading to systemic vascular endothelial cell injury, which in turn leads to a series of clinical symptoms of preeclampsia. Vascular endothelial cell injury is the central link in the etiology of preeclampsia. Among them, the imbalance of oxidation and antioxidation, the abnormal secretion of vasoactive factors, the abnormal coagulation function and the gene polymorphism or abnormal expression all play an important role in the injury of vascular endothelial cells. Now these changes and the relationship between endothelial cell damage are reviewed to explore its role in the pathogenesis of preeclampsia.