Heart disease is the leading cause of morbidity and mortality worldwide

In particular, heart failure and arrhythmias due to inherited cardiomyopathies and acquired causes such as arterial hypertension, ischemia, various stress factors or obesity put growing strain on health care systems. While significant progress in therapy of cardiovascular disease in general and heart failure in particular has been achieved in the past years, multi-drug therapy and a one-size-fits-all treatment of patients are beginning to reach limitations. To advance heart disease therapies, we see an urgent medical need for more individualized and tailored treatments in the future.

The CRC 1550, ‘Molecular Circuits of Heart Disease’ uses a novel approach that integrates the knowledge of specific causes and pathways as well as disease phenotypes by tightly intertwining experimental and patient data with systems biology and mathematical modelling approaches. By doing so, we aim to unravel the underlying molecular circuitry of heart disease, i.e. the flow of information of molecular components (DNA, RNA, proteins, lipids, metabolites), input and output signals as well as feed-forward and feedback loops, that collectively wire cardiomyocyte behavior under a variety of pathophysiological conditions. The CRC 1550 puts forward the hypothesis that each heart disease phenotype is caused by specific molecular circuits that partly overlap with other phenotype circuits. Understanding this overlap will allow us to unmask the key hubs involved in heart disease, thereby paving the way for new safe translational concepts to predict, prevent and treat heart disease.

The projects for this collaborative research center jointly address the following fundamental questions: (i) How do gene mutations result in reprogramming of cardiomyocyte function; (ii) how do stress signals affect cardiomyocyte function and their instructive signaling towards other cell populations within the heart; (iii) how do genes and environmental cues work together to shape cardiomyocyte function and dysfunction; (iv) what are the key shared molecular nodes in inherited and acquired heart disease?