Impact of endothelial-derived IncRNAs for cardiomyocyte signal transduction and the cardiac stress response (A06)

• Subject Area: Cardiology, Angiology
• Term: since 2019
• Project identifier: Deutsche Forschungsgemeinschaft (DFG) - Project number 394046768

GADLORs were found to promote myocardial fibrosis and cardiomyocyte systolic dysfunction during experimental pressure overload. Correspondingly, Lockd was identified as upregulated especially in mitotic endothelial cells, suppressing endothelial proliferation and sprouting angiogenesis. Building on these findings, project A06 will in the second funding period study endothelial-derived long-non coding RNAs as key regulators and mediators of endothelial mesenchymal activation in cardiac, but also in liver endothelial cells. The overarching goal of the project is to identify novel targets to counteract fibrosis and dysfunction in the heart and other organs.

• DFG Programme: Collaborative Research Centres
• Subproject of: SFB 1366: Vascular Control of Organ Function
• Applicant Institution: Ruprecht-Karls-Universität Heidelberg
• Project Head: Professor Dr. Jörg Heineke