Diskussionsleitung: J. Backs (Heidelberg), W. R. Bauer (Würzburg)
| (P2201) | YBX genes regulate endothelial-to-mesenchymal transition (EndMT) | |
| V. Fürle, V. Filipova, U. Laufs, J.-N. Boeckel (Leipzig) | ||
| (P2202) | Dynamics of adenosine metabolism and signalling in cardiac fibroblasts after myocardial infarction | |
| J. Hesse, J. Steinhausen, J. Bahr, Z. Ding, P. Keul, J. Schrader (Düsseldorf) | ||
| (P2203) | Fibroblast selective in vivo secretome profiling in the infarcted heart | |
| J. Bahr, G. Poschmann, A. Jungmann, M. Busch, Z. Ding, R. Zalfen, J. Steinhausen, P. Most, K. Stühler, J. Schrader (Düsseldorf, Heidelberg) | ||
| (P2204) | Single-cell RNA sequencing identifies cardiac fibroblast-derived Mannose Receptor C type 2 to control extracellular matrix turnover and renewal | |
| F. Böckling, L. Tombor, T. Rasper, W. Abplanalp, K. Schmitz, D. Leistner, D. John, A. M. Zeiher, S. Dimmeler, B. Kattih (Frankfurt am Main) | ||
| (P2205) | Concurrent Stat1 and Stat3 Signaling Modulates Tlr4/ Nfkb-mediated Immunomodulatory and Antifibrotic Effects of Cardiomyocyte-damaged Released S100a1 Protein in Cardiac Fibroblasts | |
| M. Busch, M. Daszenies, H. Klett, A. Schneider, S. Simon, J. Birkenstock, I. Dihidrisone, M. Kossack, J. Ritterhoff, M. Boerries, P. Most (Heidelberg, Freiburg) | ||
| (P2206) | Sex-dependent differences in cardiac remodelling and circulating monocyte phenotype in a model of chronic angiotensin II infusion | |
| Y. X. Shia, G. Li, S.-L. Puhl, S. Steffens (München, Würzburg) | ||
| (P2207) | Transcriptome profiling of patients' cardiac fibroblasts uncovers AEBP1 as a diagnostic and therapeutic target to counteract fibroblast activation in longstanding heart disease | |
| F. Böckling, M. Shumliakivska, L. Tombor, T. Rasper, K. Schmitz, J. Hoffmann, L. Nicin, W. Abplanalp, D. C. Carstens, M. Arsalan, F. Emrich, T. Holubec, T. Walther, D. Leistner, V. Puntmann, E. Nagel, D. John, A. M. Zeiher, S. Dimmeler, B. Kattih (Frankfurt am Main) | ||
| (P2208) | Human cardiac fibroblasts respond to the mechanical situation within the Engineered Connective Tissue (ECT), driving cell activation and fibrosis propagation. | |
| G. L. Santos, A. DeGrave, A. Hofemeier, S. A. Sisi, M. G. Setya, A. Rehman, T. Betz, W.-H. Zimmermann, S. Lutz, for the study groups: DZHK, IRTG (Göttingen) |