title: Homocysteine and arterial disease. Experimental mechanisms.
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.
authors.affiliation: Division of Vascular Surgery, Oregon Health and Sciences University, Portland, OR, USA.
authors.forename: Judith W
authors.initials: JW
authors.lastname: Cook
authors.forename: Lloyd M
authors.initials: LM
authors.lastname: Taylor
authors.forename: Susan L
authors.initials: SL
authors.lastname: Orloff
authors.forename: Gregory J
authors.initials: GJ
authors.lastname: Landry
authors.forename: Gregory L
authors.initials: GL
authors.lastname: Moneta
authors.forename: John M
authors.initials: JM
authors.lastname: Porter
mesh_terms: D000818:Animals; D001157:Arterial Occlusive Diseases / Q000097:blood / Q000378:metabolism* / Q000473:pathology; D004730:Endothelium, Vascular / Q000378:metabolism / Q000473:pathology; D006710:Homocysteine / Q000097:blood / Q000378:metabolism*; D006801:Humans
chemical_list: D006710:Homocysteine