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2015 ; 2015
(ä): 5346327
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English Wikipedia
Role for Tetrahydrobiopterin in the Fetoplacental Endothelial Dysfunction in
Maternal Supraphysiological Hypercholesterolemia
#MMPMID26697136
Leiva A
; Fuenzalida B
; Westermeier F
; Toledo F
; Salomón C
; Gutiérrez J
; Sanhueza C
; Pardo F
; Sobrevia L
Oxid Med Cell Longev
2015[]; 2015
(ä): 5346327
PMID26697136
show ga
Maternal physiological hypercholesterolemia occurs during pregnancy, ensuring
normal fetal development. In some cases, the maternal plasma cholesterol level
increases to above this physiological range, leading to maternal
supraphysiological hypercholesterolemia (MSPH). This condition results in
endothelial dysfunction and atherosclerosis in the fetal and placental
vasculature. The fetal and placental endothelial dysfunction is related to
alterations in the L-arginine/nitric oxide (NO) pathway and the arginase/urea
pathway and results in reduced NO production. The level of tetrahydrobiopterin
(BH4), a cofactor for endothelial NO synthase (eNOS), is reduced in nonpregnant
women who have hypercholesterolemia, which favors the generation of the
superoxide anion rather than NO (from eNOS), causing endothelial dysfunction.
However, it is unknown whether MSPH is associated with changes in the level or
metabolism of BH4; as a result, eNOS function is not well understood. This review
summarizes the available information on the potential link between MSPH and BH4
in causing human fetoplacental vascular endothelial dysfunction, which may be
crucial for understanding the deleterious effects of MSPH on fetal growth and
development.