Department of Pediatrics, Division of Neonatology, University of Colorado, Anschutz Medical Campus, Aurora, USA.
Department of Obstetrics and Gynecology, Division of Reproductive Sciences, University of Colorado, Anschutz Medical Campus, Aurora, USA.
Biochim Biophys Acta Mol Basis Dis. 2020 Feb 1;1866(2):165373. doi: 10.1016/j.bbadis.2018.12.024. Epub 2019 Jan 23.
The most common cause of intrauterine growth restriction (IUGR) in the developed world is placental insufficiency, a concept often used synonymously with reduced utero-placental and umbilical blood flows. However, placental insufficiency and IUGR are associated with complex, coordinated and highly regulated changes in placental signaling and nutrient transport including inhibition of insulin and mTOR signaling and down-regulation of specific amino acid transporters, Na/K-ATPase, the NaH-exchanger, folate and lactate transporters. In contrast, placental glucose transport capacity is unaltered and Ca-ATPase activity and the expression of proteins involved in placental lipid transport are increased in IUGR. These findings are not entirely consistent with the traditional view that the placenta is dysfunctional in IUGR, but rather suggest that the placenta adapts to reduce fetal growth in response to an inability of the mother to allocate resources to the fetus. This new model has implications for the understanding of the mechanisms underpinning IUGR and for the development of intervention strategies.
在发达国家，宫内生长受限（IUGR）最常见的原因是胎盘功能不全，这一概念常与子宫胎盘和脐血流减少同义。然而，胎盘功能不全和 IUGR 与胎盘信号和营养转运的复杂、协调和高度调节变化相关，包括胰岛素和 mTOR 信号抑制以及特定氨基酸转运体、Na/K-ATP 酶、NaH 交换体、叶酸和乳酸盐转运体下调。相比之下，IUGR 中胎盘葡萄糖转运能力不变，而 Ca-ATP 酶活性和参与胎盘脂质转运的蛋白质表达增加。这些发现与 IUGR 中胎盘功能失调的传统观点并不完全一致，而是表明胎盘适应于减少胎儿生长，以响应母体无法向胎儿分配资源的情况。这种新模型对理解 IUGR 的潜在机制以及干预策略的发展具有重要意义。
