Ассиметричный диметиларгинин в качестве медиатора и маркера развития эндотелиальной дисфункции
https://doi.org/10.18705/1607-419X-2007-13-2-119-127
Аннотация
Повышенный уровень АДМА в плазме крови может формироваться при умеренной форме гипергомоцистеинемии (ГГци). В большинстве случаев торможение eNOS иод, влиянием гомоцистеина возникает за счет ассиметричного диметиларгинина (АДМА), накапливающегося в эндотелиоцитах. Механизм этого явления, по-видимому, состоит в том, что гомоцистеин в клетке превращается в S-аденозилгомоцистеин - мощный ингибитор диметилар-гинин-диметиламиногидролазы (ДДАГ). Данные литературы указывают на то, что развитие эндотелиальной дисфункции может зависеть как от сочетания всех этих факторов, так и в отсутствие одного из них.
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Рецензия
Для цитирования:
Жлоба А.А. Ассиметричный диметиларгинин в качестве медиатора и маркера развития эндотелиальной дисфункции. Артериальная гипертензия. 2007;13(2):119-127. https://doi.org/10.18705/1607-419X-2007-13-2-119-127
For citation:
Zhloba A.A. ADMA as a marker and mediator of endothelial dysfunction progression. "Arterial’naya Gipertenziya" ("Arterial Hypertension"). 2007;13(2):119-127. (In Russ.) https://doi.org/10.18705/1607-419X-2007-13-2-119-127