Role for Tetrahydrobiopterin in the Fetoplacental Endothelial Dysfunction in Maternal Supraphysiological Hypercholesterolemia
Author
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Leiva, Andrea
Author
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Fuenzalida, Bárbara
Author
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Westermeier, Francisco
Author
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Toledo, Fernando
Author
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Salomón, Carlos
Author
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Gutiérrez, Jaime
Author
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Sanhueza, Carlos
Author
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Pardo, Fabián
Author
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Sobrevia, Luis
Admission date
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2019-03-18T11:53:39Z
Available date
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2019-03-18T11:53:39Z
Publication date
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2016
Cita de ítem
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Oxidative Medicine and Cellular Longevity
Volume 2016, Article ID 5346327, 10 pages
Identifier
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19420994
Identifier
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10.1155/2016/5346327
Identifier
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https://repositorio.uchile.cl/handle/2250/166696
Abstract
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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.