Ion Channels and Channelopathies

One of the principal objectives of our work is to elucidate novel molecular and cellular mechanisms of cardiac arrhythmias causing sudden cardiac death. To this end, on the one hand, our group investigates ion channel mutations found in patients and families presenting with genetic forms of lethal arrhythmias such as the congenital long QT syndrome, Brugada syndrome, or cardiac conduction disturbances. We are also interested in neurological channelopathies, particularly those related to pain syndromes and multiple sclerosis.

On the other hand, we are studying new types of regulation of cardiac ion channels relevant to arrhythmogenic mechanisms. Our group is currently investigating the regulation of the cardiac sodium channel Nav1.5 and its modulation by interacting proteins (funded by the Swiss National Science Foundation). Another focus is the TRP channel TRPM4 that is mutated in patients with cardiac conduction disorders. We are investigating the consequences of these mutations and developing new small molecule modulators of TRPM4 in the framework of the NCCR TransCure (also funded by the Swiss National Science Foundation).

Research Abriel
Fig. 1: Schematic presentation of the cardiac action potential and the three main ion channels that we are currently studying in the laboratory. The channel Nav1.5 mediates the rapid depolarization of the membrane, whereas the hERG and KCNQ1 channels are involved in the repolarization of the cardiac cell.



  • sodium channels
  • potassium channels
  • TRPM4 channels
  • cardiac electrophysiology
  • congenital long QT syndrome
  • Brugada syndrome
  • cardiac conduction defects



Prof. Hugues Abriel, MD PhD
Institute of Biochemistry and Molecular Medicine
Group leader of  Ion Channel Research 

PD Dr. Jean-Sébastien Rougier, PhD
Institute of Biochemistry and Molecular Medicine
Co-Group leader of  Ion Channel Research