Research Focus

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

We are using an integrated approach to gain a better understanding of what signaling cascades and cellular processes on the one hand and what target genes of these processes on the other 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) and to understand their involvement in disease mechanisms.

 

2) We are using chromatin-immunoprecipitation followed by genomic sequencing (ChIP-seq) to identify the target genes of epigenetic factors.

 

3) We are combining mouse genetics with experimental mouse models to investigate the physiological and pathophysiological relevance of newly identified candidate genes.

 

By following this approach we are beginning to discover signatures and key steps in the complex network of cardiac genome-environment interactions. Based on these discoveries, we ultimately aim at translating our findings to new approaches of epigenetic diagnostics and therapies in the context of cardiovascular disease.

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