Reproduction Group, Department of Physiology and Biochemistry, School of Medicine, Universidad de Antioquia, Medellín, Colombia.
Department of Obstetrics and Gynecology, School of Medicine, Universidad de Antioquia, Medellín, Colombia.
Front Endocrinol (Lausanne). 2023 May 3;14:1087845. doi: 10.3389/fendo.2023.1087845. eCollection 2023.
Preeclampsia is a pregnancy-related multisystem disorder characterized by altered trophoblast invasion, oxidative stress, exacerbation of systemic inflammatory response, and endothelial damage. The pathogenesis includes hypertension and mild-to-severe microangiopathy in the kidney, liver, placenta, and brain. The main mechanisms involved in its pathogenesis have been proposed to limit trophoblast invasion and increase the release of extracellular vesicles from the syncytiotrophoblast into the maternal circulation, exacerbating the systemic inflammatory response. The placenta expresses glycans as part of its development and maternal immune tolerance during gestation. The expression profile of glycans at the maternal-fetal interface may play a fundamental role in physiological pregnancy changes and disorders such as preeclampsia. It is unclear whether glycans and their lectin-like receptors are involved in the mechanisms of maternal-fetal recognition by immune cells during pregnancy homeostasis. The expression profile of glycans appears to be altered in hypertensive disorders of pregnancy, which could lead to alterations in the placental microenvironment and vascular endothelium in pregnancy conditions such as preeclampsia. Glycans with immunomodulatory properties at the maternal-fetal interface are altered in early-onset severe preeclampsia, implying that innate immune system components, such as NK cells, exacerbate the systemic inflammatory response observed in preeclampsia. In this article, we discuss the evidence for the role of glycans in gestational physiology and the perspective of glycobiology on the pathophysiology of hypertensive disorders in gestation.
子痫前期是一种与妊娠相关的多系统疾病，其特征为滋养细胞侵袭异常、氧化应激、全身炎症反应加重和血管内皮损伤。其发病机制包括高血压和肾脏、肝脏、胎盘和大脑的轻度至重度微血管病。其发病机制中涉及的主要机制被认为是限制滋养细胞侵袭和增加合体滋养层细胞向母体循环中释放细胞外囊泡，从而加重全身炎症反应。胎盘作为其发育的一部分以及妊娠期间母体免疫耐受表达聚糖。母胎界面上聚糖的表达谱可能在生理妊娠变化和子痫前期等疾病中发挥重要作用。目前尚不清楚聚糖及其凝集素样受体是否参与妊娠期间免疫细胞对母胎识别的机制。妊娠高血压疾病中聚糖的表达谱似乎发生了改变，这可能导致妊娠条件下胎盘微环境和血管内皮的改变，如子痫前期。母胎界面具有免疫调节特性的聚糖在早发型重度子痫前期中发生改变，这意味着先天免疫系统成分（如 NK 细胞）加重了子痫前期中观察到的全身炎症反应。本文讨论了聚糖在妊娠生理中的作用证据，以及糖生物学对视妊娠高血压疾病病理生理学的观点。
