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 language | English (US) |
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Pages (from-to) | 293-300 |
Number of pages | 8 |
Journal | Vascular Pharmacology |
Volume | 38 |
Issue number | 5 |
DOIs | |
State | Published - May 1 2002 |
Keywords
- Atherosclerosis
- Endothelial injury
- Homocysteine
ASJC Scopus subject areas
- Physiology
- Molecular Medicine
- Pharmacology