Role for Tetrahydrobiopterin in the Fetoplacental Endothelial Dysfunction in Maternal Supraphysiological Hypercholesterolemia
| PROCEDENCIA(S): | Ciencias de la Salud, USS Santiago. |
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| CATEGORÍA(S): | Biología Celular, Biología del Desarrollo, Bioquímica, Ciencias Biológicas, Endocrinología y Metabolismo, Fisiología, Hematología, Medicina Clínica, Obstetricia y Ginecología, Química Médica, Sistema Cardiovascular y Cardíaco. |
| AUTOR(ES): | Andrea Leiva / Bárbara Fuenzalida / Francisco Westermeier / Fernando Toledo / Carlos Salomón / Jaime Gutiérrez / Carlos Sanhueza / Fabián Pardo / Luis Sobrevia. |
| TIPO DE MATERIAL: | Apuntes, Artículos, Investigación. |
| ARCHIVO: |
Reconocimiento CC BY. Esta obra está bajo una Licencia Creative Commons Reconocimiento CC BY 4.0 Internacional.
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 oftetrahydrobiopterin (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.
