Han Cha, Han Lulu, Huang Pengzhu, Chen Yuanyuan, Wang Yingmei, Xue Fengxia
Department of Obstetrics and Gynecology, Tianjin Medical University General Hospital, Tianjin, China.
Front Physiol. 2019 Oct 1;10:1236. doi: 10.3389/fphys.2019.01236. eCollection 2019.
Preeclampsia is a common obstetric complication associated with pregnancy and it endangers lives of the mother and the infant. The histopathological changes associated with preeclampsia include systemic endothelial dysfunction, persistent inflammatory state, and coagulation and fibrinolysis dysregulations. Preeclampsia is considered to be caused by the systemic vasoconstriction of small arteries and disruption of the endothelial integrity, resulting in hypertension, proteinuria, and multiple organ dysfunction. However, mediators that trigger or propagate the pathology of preeclampsia remain poorly defined. Syncytiotrophoblast-derived extracellular vesicles (SDEVs) are increasingly recognized as a key mediator for the development of preeclampsia, but the underlying mechanisms through which these SDEVs are released and induce systemic responses are not fully understood. This review focuses on multiple roles of SDEVs in the pathogenesis of preeclampsia.
子痫前期是一种与妊娠相关的常见产科并发症,危及母婴生命。与子痫前期相关的组织病理学变化包括全身内皮功能障碍、持续的炎症状态以及凝血和纤溶调节异常。子痫前期被认为是由小动脉的全身血管收缩和内皮完整性破坏引起的,导致高血压、蛋白尿和多器官功能障碍。然而,引发或传播子痫前期病理过程的介质仍不清楚。合体滋养层来源的细胞外囊泡(SDEVs)越来越被认为是子痫前期发展的关键介质,但这些SDEVs释放并诱导全身反应的潜在机制尚未完全了解。本综述重点关注SDEVs在子痫前期发病机制中的多种作用。