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胎盘是介导母体与胎儿血氧、营养物质及代谢物传递的一个重要器官。根据DOHaD理论,胎儿宫内生长环境的变化会影响胎儿的发育,导致子代成年后罹患高血压病等风险增加。大量研究显示,胎盘11β-羟类固醇脱氢酶(11β-HSD2)能有效地将母体糖皮质激素在通往胎儿的过程中灭活,使胎儿免受糖皮质暴露。因此,胎盘11β-HSD2水平降低会引起胎儿宫内糖皮质激素过度暴露,导致子代成年后发生高血压病的风险显著增高。本文拟阐述胎盘11β-HSD2在胎盘中的结构和功能及其在子代成年后高血压病发生机制中的作用。深入了解胎盘11β-HSD2的变化与子代高血压病之间的关系对研究胎盘功能及代谢、产前诊断、胎源性成人疾病防治等具有重要意义。
The placenta is an important organ that mediates maternal and fetal oxygenation, nutrients and metabolites. According to DOHaD theory, changes in the environment of the fetal intrauterine growth will affect the development of the fetus, leading to an increased risk of developing hypertensive diseases in adulthood. Numerous studies have shown that placental 11β-hydroxysteroid dehydrogenase (11β-HSD2) is effective in inactivating maternal glucocorticoids during fetal access to protect the fetus from glucocorticoid exposure. Thus, a reduction in placental 11 [beta] -HSD2 levels causes excessive intrauterine glucocorticoid exposure, resulting in a significantly increased risk of developing hypertension in adulthood. This article intends to explain the structure and function of 11β-HSD2 in the placenta and its role in the pathogenesis of hypertension in adulthood. A deep understanding of the relationship between placental 11β-HSD2 changes and offspring hypertension is of great importance for the study of placental function and metabolism, prenatal diagnosis and prevention of fetal-derived adult diseases.