Recent insights into the basic mechanisms involved in atherothrombosis indicate that deleterious alterations of endothelial physiology, also referred to as endothelial dysfunction, not only represent a key early step in the development of atherosclerosis, but are also involved in plaque progression and the occurrence of atherosclerotic complications. Endothelial dysfunction is characterised by impaired endothelium-dependent vasodilation, and also by a specific state of "endothelial activation," which denotes a proinflammatory, proliferative, and procoagulatory milieu that favours all stages of atherogenesis. Dysfunction of vascular smooth muscle cells, the major cell component of the arterial wall, also contributes to atherosclerosis; impairment in smooth muscle cell turnover and extra-cellular matrix synthesis are among the major determinants of atherosclerotic plaque stability.

The aim of this EVGN priority area is to define the molecular mechanisms underlying endothelial and smooth cell dysfunction and discover new preventive strategies.

• Endothelial Dysfunction (for general public)
• Endothelial dysfunction programme within EVGN (for specialists)