Homocysteine metabolism, hyperhomocysteinaemia and vascular disease: An overview

R. Castro, I. Rivera, H. J. Blom, C. Jakobs, I. Tavares de Almeida

Research output: Contribution to journalReview article

199 Scopus citations

Abstract

Hyperhomocysteinaemia has been regarded as a new modifiable risk factor for atherosclerosis and vascular disease. Homocysteine is a branch-point intermediate of methionine metabolism, which can be further metabolised via two alternative pathways: degraded irreversibly through the transsulphuration pathway or remethylated to methionine by the remethylation pathway. Both pathways are B-vitamin-dependent. Plasma homocysteine concentrations are determined by nongenetic and genetic factors. The metabolism of homocysteine, the role of B vitamins and the contribution of nongenetic and genetic determinants of homocysteine concentrations are reviewed. The mechanisms whereby homocysteine causes endothelial damage and vascular disease are not fully understood. Recently, a link has been postulated between homocysteine, or its intermediates, and an alterated DNA methylation pattern. The involvement of epigenetic mechanisms in the context of homocysteine and atherosclerosis, due to inhibition of transmethylation reactions, is briefly overviewed.

Original languageEnglish (US)
Pages (from-to)3-20
Number of pages18
JournalJournal of Inherited Metabolic Disease
Volume29
Issue number1
DOIs
StatePublished - Feb 1 2006

All Science Journal Classification (ASJC) codes

  • Genetics
  • Genetics(clinical)

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