Homocysteine and arterial disease: Experimental mechanisms

Judith W. Cook, Lloyd M. Taylor, Susan L. Orloff, Gregory J. Landry, Gregory L. Moneta, John M. Porter

Research output: Contribution to journalArticle

36 Scopus citations

Abstract

Hyperhomocysteinemia (hH(e)) in the general population is associated with incidence and progression of arterial occlusive disease, although the underlying mechanisms are not well defined. Current research supports a role for homocysteine (H(e))-mediated endothelial damage and endothelial dysfunction. This mechanism appears to be a key factor in subsequent impaired endothelial-dependent vasoreactivity and decreased endothelium thromboresistance. These consequences may predispose hyperhomocysteinemic vessels to the development of increased atherogenesis. Additional mechanisms of H(e)-mediated vascular pathology, including protein homocysteinylation and vascular smooth muscle cell proliferation may also play a role. Continued investigation into the mechanisms contributing to H(e) toxicity will provide further insight into the processes by which hH(e) may increase atherosclerosis.

Original languageEnglish (US)
Pages (from-to)293-300
Number of pages8
JournalVascular Pharmacology
Volume38
Issue number5
DOIs
StatePublished - May 1 2002

Keywords

  • Atherosclerosis
  • Endothelial injury
  • Homocysteine

ASJC Scopus subject areas

  • Physiology
  • Molecular Medicine
  • Pharmacology

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