eNOS and Nitric Oxides Signaling

Altered endothelial cell function is recognized as the initiating event of many cardiovascular and metabolic diseases. We study global changes in endothelial cell signaling pathways essential for the regulation of vascular homeostasis and the initiation and progression of cardiovascular and metabolic diseases, making use of cutting-edge transcriptomic, proteomic and metabolomic technologies.

Recent work linked the endothelium-derived gasotransmitter nitric oxide, glucose metabolism and antioxidant responses against the development of hypertension and atherosclerosis. It was possible to demonstrate that NO bioavailability is regulated through the tyrosine phosphorylation of eNOS and that enhancing eNOS activity e.g. through inhibition of the tyrosine phosphatase VE-PTP, represents a novel therapeutic option for patients with cardiovascular disease. Several lines of evidence indicated the presence of eNOS in the nucleus of endothelial cells. Current projects investigate the epigeNOmic regulation of endothelial gene expression and metabolism.