Role for tetrahydrobiopterin in the fetoplacental endothelial dysfunction in maternal supraphysiological hypercholesterolemia

Leiva, Andrea, Fuenzalida, Barbara, Westermeier, Francisco, Toledo, Fernando, Salomon, Carlos, Gutierrez, Jaime, Sanhueza, Carlos, Pardo, Fabian and Sobrevia, Luis (2016) Role for tetrahydrobiopterin in the fetoplacental endothelial dysfunction in maternal supraphysiological hypercholesterolemia. Oxidative Medicine and Cellular Longevity, 2016 . doi:10.1155/2016/5346327


Author Leiva, Andrea
Fuenzalida, Barbara
Westermeier, Francisco
Toledo, Fernando
Salomon, Carlos
Gutierrez, Jaime
Sanhueza, Carlos
Pardo, Fabian
Sobrevia, Luis
Title Role for tetrahydrobiopterin in the fetoplacental endothelial dysfunction in maternal supraphysiological hypercholesterolemia
Journal name Oxidative Medicine and Cellular Longevity   Check publisher's open access policy
ISSN 1942-0994
1942-0900
Publication date 2016
Sub-type Critical review of research, literature review, critical commentary
DOI 10.1155/2016/5346327
Open Access Status DOI
Volume 2016
Total pages 11
Place of publication New York, NY, United States
Publisher Hindawi Publishing Corporation
Collection year 2017
Language eng
Formatted abstract
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.
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Critical review of research, literature review, critical commentary
Collections: UQ Centre for Clinical Research Publications
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