AG Clauß

AG Clauss - Experimental and translational electrophysiology

In the Clauss group, we investigate mechanisms that lead to arrhythmias. From genetic, molecular and cellular signaling pathways to autonomic and immunological influences, we aim to understand what drives proarrhythmic remodeling. A deeper understanding of these processes will help us to identify the signaling pathways that contribute to the development of arrhythmias and, based on this, to develop and test new therapeutic strategies. The combination of our findings from in vitro, mouse and pig models enables us to translate research results into clinical practice.

Current projects

Myeloid interactions in cardiovascular diseases

Work of the Clauss group together with our cooperation partners implicates cardiac resident macrophages (CRMs) in physiological conduction through the AV node (Hulsmans & Clauss, Cell, 2017). This results in an electrical coupling of CRMs and cardiomyocytes via connexin-43 gap junctions, whereby CRMs regulate conduction through the AV node.

The translation of this discovery to pathological processes identified recruited macrophages as an important factor in the pathogenesis of atrial fibrillation (Hulsmans et al., Science, 2023). However, it remains a major challenge to translate these results from mouse experiments into the clinic. This is partly due to the difference in heart size between mice and humans, which is an important factor in arrhythmia development.

With the help of our HOMER(Hypertension, Obesity, Mitral Regurgitation) pig model for atrial fibrillation, we aim to close the current gaps in the pathogenesis, identify new mechanisms and counteract these with specially developed therapies.