Our research is focused on the process of cardiac remodeling. Volume- or pressure-overload in the heart (e.g. caused by valvular heart disease or myocardial infarction) causes an initial adaptive response, leading to stabilization of the cardiovascular system. Over time, the adaptive remodeling processes progresses into a maladaptive outcome leading to a deterioration of heart function and finally to heart failure.
We are particularly interested to understand the mechanisms underlying the transition of cardiac remodeling from compensated hypertrophy with retained heart function to heart failure in order to develop new therapeutic strategies, focusing on load-depended remodeling and the analysis of epigenetic regulation of these processes.