© 2003 by European Society of Cardiology
Copyright © 2003, European Society of Cardiology
Adenosine—the missing link to understanding homocysteine pathogenicity or more smoke on the horizon?
Department for Physiology, Medical Faculty Carl Gustav Carus, Technical University of Dresden, Fetscherstrasse 74, D-01307 Dresden, Germany
* Tel.: +49-351-458-6030; fax: +49-351-458-6301. andreas.deussen@mailbox.tu-dresden.de
Received 30 May 2003; revised 4 June 2003; accepted 5 June 2003
| The first 10% of the full text of this article appears below. |
See article by Riksen et al. [8] (pages 271–276) in this issue.
Based on epidemiological studies, homocysteine (Hcy) is regarded as an independent risk indicator for occlusive vascular diseases [1,2]. Under experimental conditions, increased Hcy concentrations have been found to result in endothelial dysfunction, leukocyte adhesion, and smooth muscle and collagen proliferation [3–6]. However, the underlying molecular and metabolic links have not been conclusively elucidated [7]. Thus, it still remains to be determined whether Hcy indeed represents a risk factor or rather a risk indicator.
In this issue of the Journal, Riksen et al. [8] present a new hypothesis on the relationship of Hcy and some of its presumed effects. This hypothesis is centered on the metabolism of Hcy