CRC1366

During the exposure to abnormal loading conditions, cardiac endothelial cells (EC) undergo a transient mesenchymal activation process, in which they proliferate and upregulate extracellular matrix genes and could thereby promote heart failure. The role of EC mesenchymal activation for cardiac fibrosis and dysfunction remains similarly unknown as its crucial regulators and mediators. Here, we investigate the role of the largely unknown EC derived lncRNA Gadlor1/Gadlor2 and Lockd for cardiac fibrosis and dysfunction, and will unravel the pro-fibrotic molecular mechanisms of these lncRNAs. Moreover, we will conduct a large scale RNAi screen to find new regulators of EC mesenchymal activation that – like the lncRNAs – could serve as therapeutic target in the future.