Zhang Song, Regnault Timothy R H, Barker Paige L, Botting Kimberley J, McMillen Isabella C, McMillan Christine M, Roberts Claire T, Morrison Janna L
Early Origins of Adult Health Research Group, Sansom Institute for Health Research, University of South Australia, Adelaide, SA 5001, Australia.
Departments of Obstetrics and Gynecology, University of Western Ontario, London, ON N6A 5C1, Canada.
Nutrients. 2015 Jan 8;7(1):360-89. doi: 10.3390/nu7010360.
The placenta is the primary interface between the fetus and mother and plays an important role in maintaining fetal development and growth by facilitating the transfer of substrates and participating in modulating the maternal immune response to prevent immunological rejection of the conceptus. The major substrates required for fetal growth include oxygen, glucose, amino acids and fatty acids, and their transport processes depend on morphological characteristics of the placenta, such as placental size, morphology, blood flow and vascularity. Other factors including insulin-like growth factors, apoptosis, autophagy and glucocorticoid exposure also affect placental growth and substrate transport capacity. Intrauterine growth restriction (IUGR) is often a consequence of insufficiency, and is associated with a high incidence of perinatal morbidity and mortality, as well as increased risk of cardiovascular and metabolic diseases in later life. Several different experimental methods have been used to induce placental insufficiency and IUGR in animal models and a range of factors that regulate placental growth and substrate transport capacity have been demonstrated. While no model system completely recapitulates human IUGR, these animal models allow us to carefully dissect cellular and molecular mechanisms to improve our understanding and facilitate development of therapeutic interventions.
胎盘是胎儿与母亲之间的主要界面，通过促进底物转运和参与调节母体免疫反应以防止对胚胎的免疫排斥，在维持胎儿发育和生长方面发挥着重要作用。胎儿生长所需的主要底物包括氧气、葡萄糖、氨基酸和脂肪酸，它们的转运过程取决于胎盘的形态特征，如胎盘大小、形态、血流和血管分布。包括胰岛素样生长因子、细胞凋亡、自噬和糖皮质激素暴露等其他因素也会影响胎盘生长和底物转运能力。宫内生长受限（IUGR）通常是功能不全的结果，与围产期发病率和死亡率的高发生率相关，以及成年后期心血管和代谢疾病风险增加有关。已经使用了几种不同的实验方法在动物模型中诱导胎盘功能不全和IUGR，并证明了一系列调节胎盘生长和底物转运能力的因素。虽然没有一个模型系统能完全重现人类IUGR，但这些动物模型使我们能够仔细剖析细胞和分子机制，以增进我们的理解并促进治疗干预措施的开发。
