Project A03

Reactive oxygen species (ROS) are important signals generated in response to damage. The project will identify the metabolic consequences of increased ROS in particular with respect to the inactivation of the enzyme Nitrilase Family Member 2 (NIT2) and how this affects endothelial function. The consequence of cell-specific increased ROS in a transgenic model of D-amino acid oxidase expression for the damage response of the stroma-vascular compartment will be determined in co-culture but also animal experiments. For the latter, carotid artery wire injury and myocardial infarction will be applied and intercellular redox cross talk will be determined by time-resolved single cell RNA-sequencing.