Homocysteine and vascular disease
Nature MedicinePublished 1 April 1996
Kevin K. McCully
Citations697
SJR quartileQ1
SJR score18.33
SNIP8.71
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TL;DR
The discovery of hyperhomocysteinemia as a major factor in the pathogenesis of arteriosclerosis offers new strategies and opportunities for prevention and treatment.
Abstract
The discovery of hyperhomocysteinemia as a major factor in the pathogenesis of arteriosclerosis offers new strategies and opportunities for prevention and treatment.
Keywords
Medicine
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A strong association between homocysteine concentration and folate, vitamin B12, and vitamin B6 status, as well as age is indicated, suggesting that a substantial majority of the cases of high homocy steine in this older population can be attributed to vitamin status.
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The totally automated fluorescence polarization immunoassay for homocyst(e)ine with no pretreatment or chromatographic steps is developed and exhibited almost no cross-reactivity towards cysteine and methionine.
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Homocysteine thiolactone, released from homocysteinylated LDL within vascular wall, promotes intimal injury, oxidation of cholesterol and unsaturated lipids, platelet aggregation, thrombogenic factors, myointimal hyperplasia, deposition of sulfated glycosaminoglycans, fibrosis and calcification of atherosclerotic plaques.
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123 Citations1976Yashpal S. Kanwar, José R. Manaligod +1 more
The morphologic abnormalities under light or electron microscopy in this patient with 5,10-methylenetetrahydrofolate reductase deficiency were strikingly similar to those reported in patients with cystathionine-β-synthase deficiency and with N5-methyltetrahYDro Folate homocystine methyltransfcrase deficiency.
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Long-term vitamin supplementation may be required in some individuals to prevent hyperhomo-cysteinemia, and substitution of vitamin supplementation by dietary guidelines to increase folate intake from food products failed to maintain normal plasma homocysteine levels in participants from subgroup B.
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These findings relate an area of sulfur amino acid metabolism to the physiological action of growth hormone, accelerated growth in homocystinuria, initiation of arteriosclerosis, and control of cellular growth.
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In a group of young post-myocardial infarction patients the in vitro susceptibility of LDL to oxidative modification was found to be significantly related to the severity of coronary atherosclerosis as assessed by angiography, and the initial results support the notion that oxidation of LDL also may be of clinical relevance.