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From the Department of Internal Medicine, University of Iowa College of Medicine, Iowa City.
Correspondence to Frank M. Faraci, PhD, University of Iowa College of Medicine, Department of Internal Medicine, E329-2 GH, Iowa City, IA 52242. E-mail frank-faraci@uiowa.edu
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
Studies of endothelium remain a cornerstone of research in vascular biology, having very broad potential and implications. At a basic level, this research attempts to understand the intricacies of normal biology of endothelial cells. Such knowledge should provide the foundation for understanding molecular mechanisms that contribute to and protect from endothelial dysfunction in disease states. Ultimately, this effort will very likely foster the development of more effective and increasingly novel therapies for cardiovascular disease.
See page 729
Endothelial dysfunction is present in all forms of cardiovascular disease as well as in Alzheimers disease and during aging. The impact of endothelial dysfunction in pathophysiology is gaining ever increasing recognition, including strong evidence that impaired endothelial function is an independent predictor of cardiovascular events. At one level are now classic examples such as the role of abnormal endothelial function in development of atherosclerosis and thrombosis. At another level are more diverse consequences when organ- and tissue-specific effects are considered. For example, emerging evidence suggests that endothelial dysfunction in the cerebral circulation may contribute to cognitive impairment and dementia.
With this issue, Arteriosclerosis, Thrombosis, and Vascular Biology initiates a series of Brief Reviews on endothelium. The intent is to highlight selected areas of research in endothelial cell biology that will be of broad interest and are areas of study in which rapid advances are underway. The first review in this series is by Wolfrum et al1 and focuses on endothelium-dependent effects of statins, inhibitors of HMG-CoA reductase. Future reviews in the series will
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