The Link Between Hyperhomocysteinemia and Hypomethylation: Implications for Cardiovascular Disease
J. inborn errors metab. screen
;
5: e160024, 2017. graf
Artigo
em Inglês
|
LILACS-Express
| LILACS
| ID: biblio-1090944
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:
DisponíveL
Índice:
LILACS (Américas)
Tipo de estudo:
Fatores de risco
Idioma:
Inglês
Revista:
J. inborn errors metab. screen
Assunto da revista:
Medicina Cl¡nica
/
Patologia
Ano de publicação:
2017
Tipo de documento:
Artigo
/
Documento de projeto
País de afiliação:
Portugal
/
Estados Unidos
Instituição/País de afiliação:
Harvard Medical School/US
/
Universidade de Lisboa/PT
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