The Link Between Hyperhomocysteinemia and Hypomethylation: Implications for Cardiovascular Disease
J. inborn errors metab. screen
; 5: e160024, 2017. graf
Article
em En
|
LILACS-Express
| LILACS
| ID: biblio-1090944
Biblioteca responsável:
BR1.1
ABSTRACT
Abstract Increased levels of homocysteine have been established as a risk factor for cardiovascular disease (CVD) by mechanisms still incompletely defined. S-Adenosylhomocysteine (SAH) is the metabolic precursor of homocysteine that accumulates in the setting of hyperhomocysteinemia and is a negative regulator of most cell methyltransferases. Several observations, summarized in the current review, support the concept that SAH, rather than homocysteine, may be the culprit in the CVD risk that has been associated with hyperhomocysteinemia. This review examines the biosynthesis and catabolism of homocysteine and how these pathways regulate accumulation of SAH. In addition, the epidemiological and experimental links between hyperhomocysteinemia and CVD are discussed, along with the evidence suggesting a role for SAH in the disease. Finally, the effects of SAH on the hypomethylation of DNA, RNA, and protein are examined, with an emphasis on how specific molecular targets may be mediators of homocysteine-associated vascular disease.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
LILACS
Tipo de estudo:
Risk_factors_studies
Idioma:
En
Revista:
J. inborn errors metab. screen
Assunto da revista:
Medicina Cl¡nica
/
Patologia
Ano de publicação:
2017
Tipo de documento:
Article
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Project document
País de afiliação:
Portugal
/
Estados Unidos