Homocysteine and arterial disease: Experimental mechanisms
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- 作者：Cook ; Judith W. ; Taylor Jr ; Lloyd M. ; Orloff ; Susan L. ; Landry ; Gregory J. ; Moneta ; Gregory L. ; et. al.
- 关键词：Homocysteine ; Atherosclerosis ; Endothelial injury
- 刊名：Vascular Pharmacology
- 出版年：2002
- 出版时间：May, 2002
- 年：2002
- 卷：38
- 期：5
- 页码：293-300
- 全文大小：144 K
文摘
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.