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The development of atherosclerosis is a complex, multi-step process, which is at least in part controlled by the functional state of the vascular endothelium. It is generally believed that the functional state of the endothelium is influenced by a broad set of cardiovascular risk factors and that endothelial dysfunction is the stereotypic cellular response to a broad range of different stimuli on the background of a poorly defined genetic predisposition.1That such a concept represents an over-simplification has become evident through studies demonstrating maternal–foetal transmission of the atherosclerotic risk2 and ‘atherosclerotic programming’ of cells derived from mice with a pro-atherosclerotic phenotype.3 Such programming is the consequence of epigenetic modifications like DNA methylation or histone acetylation, processes that are controlled by several different enzyme families.One of these enzymes, SIRT1, a class III histone deacetylase (HDAC), has gained considerable interest as a mediator of longevity induced by caloric restriction.4 Also in the vascular system, SIRT1 has been … *Corresponding author. Tel: +49 69 6301 6995; fax: +49 69 6301 7668. E-mail address: r.brandes{at}em.uni-frankfurt.de

Activating SIRT1: a new strategy to prevent atherosclerosis?