Complex, coordinated and highly regulated changes in placental signaling and nutrient transport capacity in IUGR

BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE

卷:1866

Review

Chassen, Stephanie¹  Jansson, Thomas² 

[1] Univ Colorado, Dept Pediat, Div Neonatol, Anschutz Med Campus, Aurora, CO 80045 USA

[2] Univ Colorado, Dept Obstet & Gynecol, Div Reprod Sci, Anschutz Med Campus, Aurora, CO 80045 USA

关键词: Syncytiotrophoblast;    Placental transport;    Fetal growth restriction;    Human;    Maternal-fetal exchange;    Fetal development;   

DOI  :  10.1016/j.bbadis.2018.12.024

来源: Elsevier

【 摘 要 】

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 Na+/H+-exchanger, folate and lactate transporters. In contrast, placental glucose transport capacity is unaltered and Ca2+-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.

【 授权许可】

Free