We want to be able to predict and prevent triggers of arrhythmic events, and to use the beneficial effects of exercise on electrophysiological remodeling in a safe manner. We especially focus on the role of Ca2+ handling by cardiac proteins associated with the sarcoplasmic reticulum, such as RyR2, SERCA2 and CaMKII. To better understand the role of these proteins, we use rodent models of heart failure, CPVT, HCM and ischemia-reperfusion. We combine clinical observations and interventions with molecular biology, cellular electrophysiology, Langendorff-perfused hearts and in vivo characterization by echocardiography, MRI and telemetric ECG recording. We also expose rodent models to exercise training by voluntary running in resistance-controlled running wheels and treadmills. This is possible because the personnel in our group have different academic backgrounds and specific know-how, from nanotechnology and molecular biology to clinical training in cardiology. We work together to identify key parts in the processes that lead to cardiac disease, and to develop strategies for future therapies.
- Antiarrhythmic effects of exercise training
- Mechanisms and therapeutic strategies for arrhythmias in CPVT
- Novel therapeutic targets for arrhythmias induced by ischemia and reperfusion
- Beneficial effects of exercise training in hypertrophic cardiomyopathy