Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Homocyst(e)ine elevation is associated with a two- to threefold fold increased risk of ischemic stroke. Although most commonly associated with large-artery atherosclerosis and venous thrombosis, hyperhomocysteinemia may contribute to stroke by other mechanisms as well. Levels of homocysteine are determined by genetic regulation of the enzymes involved in homocyst(e)ine metabolism and by levels of the vitamin cofactors (folate, B (6), and B (12)) associated with those reactions. Emerging evidence suggests that genetic variation within this pathway, such as the methyleneterahydrofolate reductase and cystathionine beta-synthase and nicotinamide N-methyltransferase genes, increases the risk of ischemic stroke. The introduction of grain folate fortification in 1998 has reduced homocyst(e)ine concentrations in the U.S. population. However, it is important to screen for vitamin B (12) deficiency and be cognizant that vitamin B (6) levels may be low in the elderly and in individuals with inflammatory disorders. The Vitamin Intervention in Stroke Prevention study failed to prove that high-dose supplementation with folate, B (6), and B (12) reduced the risk of recurrent stroke or myocardial infarction at 2 years; however, there is an ongoing clinical trial evaluating the potential benefit of vitamin supplementation.
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PMID:Homocyst(e)ine and stroke. 1647 41

Cardiovascular disease (CVD) is extremely complex. It results from the interaction of many genetic and environmental factors. Several studies have demonstrated its genetic basis, estimating a heritability of approximately 60%. In the last 5 years, at least 19 genome-wide explorations for genes related to CVD have been undertaken, but none has yet unequivocally demonstrated a causal relationship with the disease. One method that can be used to find the causative genes is analyzing intermediate genetic phenotypes or risk factors, such as plasma homocysteine (Hcy). A recent genome-wide quantitative-trait-linkage analysis of Hcy plasma levels has found a previously unsuspected gene as the major genetic determinant of this risk factor. It codes for the enzyme nicotinamide N-methyltransferase, and this gene is now a candidate gene that explains a portion of the genetic basis of CVD. If confirmed, this finding will probably influence future research on the mechanisms underlying atherosclerosis and CVD, as well as other complex diseases related to plasma Hcy levels, such as Alzheimer's disease and osteoporosis.
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PMID:Plasma homocysteine and the genetics of cardiovascular disease. 1980 73