Vascular inflammation and remodelling
Cardiovascular diseases remain the main cause of mortality and morbidity in Western societies, most notably as a consequence of myocardial infarction and stroke. The remodeling of arteries preceding and following the myocardial infarction is a pivotal event in these pathological processes. Inflammatory cells of the innate immune system play an essential role in these processes through production of inflammatory mediators and growth promoting factors. The phenotype of these cells is heavily influenced by both the genetic make-up of the individual patient and the known life-style based risk factors for cardiovascular disease.
Therefore, we approach this challenge by employing 'functional genomics', to identify key molecules in both pathological and beneficial arterial remodeling. Our goal is to enable future 'personalized medicine' where diagnostic molecular profiling in individual patients will be followed by a targeted, individual molecular treatment.
Boon RA, et al. & Horrevoets AJ: KLF2-induced actin shear fibers control both alignment to flow and JNK signaling in vascular endothelium. Blood. 2010; 115:2533-2542.
Rohlena J, et al & Horrevoets AJ: Endothelial CD81 is a marker of early human atherosclerotic plaques and facilitates monocyte adhesion. Cardiovasc Res. 2009;81:187-196.
Schirmer SH, et al & Horrevoets AJG, van Royen N.: Interferon-beta signalling is enhanced in patients with insufficient coronary collateral artery development and inhibits arteriogenesis in mice. Circ Res. 2008;102:1286-1294.
Fledderus JO, et al. & Horrevoets AJ. Prolonged shear stress and KLF2 suppress constitutive pro-inflammatory transcription through inhibition of ATF2. Blood. 2007;109:4249-4257.
Dekker RJ, et al. & Horrevoets AJG : KLF2 provokes a gene expression pattern that establishes functional quiescent differentiation of the endothelium. Blood. 2006;107:4354-4363.
Overview of publications of Anton Horrevoets Group: http://www.ncbi.nlm.nih.gov/pubmed/?term=horrevoets+aj
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