Julio Saez-Rodriguez, from the German Centre for Cardiovascular Research (DZHK), Heidelberg/Mannheim site, is the senior author of the publication and a professor at Heidelberg University. His team analyzed data from 25 studies involving more than 1,500 patients, creating a unified “map” of gene activity in heart tissue. This revealed that, in cases of heart failure, similar genetic programs are activated across different cell types—regardless of the underlying cause of the disease.
Fibroblasts, a type of connective tissue cell, play a central role in this process. They emit signals that influence the behavior of cardiac muscle cells. This cellular communication drives characteristic remodeling processes in the heart, such as scar tissue formation and thickening of the heart muscle.
Pathological patterns partially reverse
The researchers also found that these pathological patterns can partially reverse with successful treatment. Thus, changes in gene activity reflect not only the disease itself but also the recovery of heart function.
With this new reference map, researchers now have a tool that enables the study of heart failure on an entirely new level. It allows for the analysis of interactions between cell types within the heart and the identification of new therapeutic targets.
The project was conducted in collaboration with Heidelberg University, the DZHK, and the European Bioinformatics Institute (EMBL-EBI). The results are publicly accessible via the online platform ReHeaT.
Originalpublikation: Lanzer JD, Ramirez Flores RO, Liñares Blanco J, et al. A cross-study transcriptional patient map of heart failure defines conserved multicellular coordination in cardiac remodeling. Nat Commun. 2025;16(1):9659. Published 2025 Oct 31. doi:10.1038/s41467-025-62219-6
