Open AccessMethylenetetrahydrofolate Reductase Polymorphism, Plasma Folate, Homocysteine, and Risk of Myocardial Infarction in US Physicians
Author(s) -
Jing Ma,
Meir J. Stampfer,
Charles H. Hennekens,
Phyllis Frosst,
Jacob Selhub,
Jonathan Horsford,
M.R. Malinow,
Walter C. Willett,
Rima Rozen
Publication year - 1996
Publication title -
circulation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.795
H-Index - 607
eISSN - 1524-4539
pISSN - 0009-7322
DOI - 10.1161/01.cir.94.10.2410
Subject(s) - methylenetetrahydrofolate reductase , homocysteine , hyperhomocysteinemia , genotype , medicine , transsulfuration , myocardial infarction , endocrinology , methionine , risk factor , case control study , gastroenterology , cystathionine beta synthase , genetics , biology , gene , amino acid
Hyperhomocysteinemia appears to be an independent risk factor for coronary disease. Elevated levels of plasma total homocysteine (tHCY) can result from genetic or nutrient-related disturbances in the transsulfuration or remethylation pathways for homocysteine metabolism. The enzyme 5,10-methylenetetrahydrofolate reductase (MTHFR) catalyzes the reduction of 5,10-methylenetetrahydrofolate to 5-methyltetrahydrofolate, the predominant circulatory form of folate, which serves as a methyl donor for remethylation of homocysteine to methionine. A common mutation in MTHFR recently has been identified.
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