SFB 834: Endothelial Signalling and Vascular Repair

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Endothelial activation or “dysfunction” is generally accepted to be one of the earliest measurable changes to take place within vessels during cardiovascular disease development and there is a well-documented relationship between attenuated endothelial function and poor patient prognosis. The mechanisms that contribute to the development of endothelial dysfunction have been investigated in detail but the protective molecular mechanisms that maintain the vasculature in a healthy state remain largely elusive. Moreover, it is unclear how endogenous cellular repair mechanisms/processes can improve endothelial cell function and neovascularisation. Our Collaborative Research Centre (hereafter referred to as SFB 834) aims to identify the molecular mechanisms and cellular mediators that determine endothelial cell function and repair in a series of basic science, translational and clinical projects. The overall long-term goal is the development of new therapeutic concepts and their transfer to the clinic. The projects making up SFB 834 are grouped under two general headings: projects in part A: “Endothelial Signaltransduktion”, focus largely on specific signalling molecules and molecular mechanisms that are necessary for the maintenance of endothelial function. The projects in part B “Endothelial Cell Function and Repair” are translational research projects that aim to elucidate the interaction between risk factors (especially those associated with altered cellular metabolism) and endothelial function and to improve the treatment of cardiovascular disease by cell therapy. Several projects focus on the detailed analysis of molecules and established signalling pathways such as nitric oxide, reactive oxygen species, G-protein coupled receptors etc. to gain novel insight into their regulation and participation in cardiovascular disease. However, SFB 834 has a history of identifying emerging priority areas and studying their applicability to vascular research at the basic science and translational research levels. Thus, a subsection of projects focuses on novel mechanisms of epigenetic regulation including regulators of histone modification, microRNAs, long non coding RNAs and RNA splicing. We believe that the elucidation of these novel emerging topics will provide crucial insights into the epigenetic control of cardiovascular diseases, which may lead to the discovery of novel therapeutic targets. It is this focus on the physiology and pathophysiology of the vessel wall and the integration of endothelial cell signalling, vascular repair and translational research that characterises SFB 834.