Several forms of stress such as neurohormonal activation, metabolic disarrangements or inflammatory outbreaks drive the development of cardiovascular diseases. Our research focuses on unraveling the molecular basis of the interaction between these stressors and the cardiac genome. An intact and functional cardiac myocyte is regulated by a fine-tuned and concerted action of a multitude of signaling events that culminate in coordinated gene expression programs. However, disturbances in the complex interplay between metabolism, inflammation, calcium handling, signaling molecules, transcription factors and epigenetic regulators lead to alterations in gene expression that promote myocardial disease.

We apply an integrated approach to gain a better understanding of what signaling cascades and cellular processes on the one hand and target genes of these processes on the other hand are involved in different aspects of myocardial disease.

1. We are using molecular biology techniques, biochemistry and cell biology to identify interaction partners of chromatin-modifying enzymes such as histone deacetylases (HDACs) in order to understand their role in disease development.
2. We are using OMICs approaches such as RNAseq, ChIPseq and Mass Spectrometry to identify cellular targets of epigenetic factors and to unravel their involvement in the regulation of myocardial function.
3. We are using genetic model systems to investigate the physiological and pathophysiological relevance of newly identified candidate genes.

By following this approach we have begun to discover signatures and molecular hubs in the complex network of cardiac genome-environment interactions. Based on these discoveries, we ultimately aim at translating our findings into new epigenetic diagnostics and therapies in the context of cardiovascular diseases.