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- W1567793348 endingPage "300" @default.
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- W1567793348 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." @default.
- W1567793348 created "2016-06-24" @default.
- W1567793348 creator A5003579169 @default.
- W1567793348 creator A5017698587 @default.
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- W1567793348 creator A5071937178 @default.
- W1567793348 creator A5076128617 @default.
- W1567793348 creator A5088788407 @default.
- W1567793348 date "2002-05-01" @default.
- W1567793348 modified "2023-10-13" @default.
- W1567793348 title "Homocysteine and arterial disease" @default.
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- W1567793348 doi "https://doi.org/10.1016/s1537-1891(02)00254-9" @default.