Flavien Charpentier PhD Cardiac Electrophysiology
Course and current status
Inserm Research Director
"Cardiac diseases and sudden death" team leader
Inserm UMR1087, CNRS UMR6291 (Director: Hervé Le Marec)
L'institut du thorax
8 quai Moncousu
44007 Nantes cedex 1
tel. +33 228 08 01 10
fax +33 228 08 01 30
- 1991: PhD of the University of Nantes, section "Health and life sciences
- 2003: Authorization to lead researches, University of Nantes
- 2008-2011: leader of team I "Cardiac diseases and sudden death" (CNRS ERL3147), Inserm UMR915, Nantes
- 2004-2008: co-leader of team IIc, Inserm UMR 533, Nantes
- 1996-2008: Inserm Research Scientist, Inserm CJF96-01 and UMR533, Nantes
- 1994-1996: post-doctoral research scientist, URA CNRS 1340, Nantes
- 1991-1994: post-doctoral research scientist, Columbia University, New York
- Member of the evaluation committee of the Inserm/DHOS funding program on clinical and translational research (since 2010)
- Member of the evaluation committee of the French National Research Agency (ANR) for the GENOPAT funding program (2008-2009)
- Expert for the French Agency for the Evaluation of Research and University Teaching (AERES; since 2008)
- Member of the Scientific Council of the Fondation de l’Avenir (since 2009)
- Member of the editorial boards of the Journal of Molecular and Cellular Cardiology (since 2008), Frontiers in Cardiac Electrophysiology (since 2010) and Europace (since 2012)
- Referee for Circulation, Circulation Research, Cardiovascular Research, Journal of Molecular and Cellular Cardiology, British Journal of Pharmacology, American Journal of Physiology, Trends in Cardiovascular Medicine, Journal of Cardiovascular Pharmacology, Frontiers in Cardiac Electrophysiology…
- Expert for the Association Française contre les Myopathies (AFM), the CORDDIM, the CNRS, the Dutch Heart Foundation, the Israel Science Foundation and Research Foundation Flanders.
Organization of scientific meetings
- Co-organizer of the 36th annual meeting of the European Working Group on Cardiac Cellular Electrophysiology, 15-16/09/12, Nantes, France.
- Co-organizer of the Denis Escande international symposia, 22/06/07, 29-30/06/09, 16-17/06/11, Nantes, France.
Recent representative lectures
- Nav1.5, cardiac arrhythmias and cardiomyopathies. 07/10/10. Montreal Cardiology Institute, Montreal, Canada.
- The cardiac sodium channel and its role in arrhythmogenic remodeling. 24/06/11, EUTrigTreat General Assembly, Utrecht, the Netherlands.
- Animal models of cardiac arrhythmias. 21/09/11. 4th Asia Pacific Heart Rhythm Society Scientific Sessions, Fukuoka, Japan.
- Sodium channel abnormalities and cardiac conduction diseases. 01/04/12. Frontiers in CardioVascular Biology 2012, London, UK.
Sudden cardiac death claims 500 000 deaths annually in Europe, ventricular fibrillation being the main underlying arrhythmia. By performing synergistic studies in molecular and clinical genetics, in molecular and cellular physiology and in transgenic animals, our team elucidated the mechanisms of rare monogenic arrhythmias and improved our understanding of the molecular basis of normal and abnormal cardiac electrical activity. We and others also showed that loss-of-function mutations of the gene encoding Nav1.5 cardiac Na+ channel, can lead to structural cardiac diseases, i.e. exacerbated aging-related fibrosis and/or dilated cardiomyopathy (DCM). Part of our current projects is aimed at investigating the mechanisms of these degenerative diseases. In parallel, we established promising models of heart failure with preserved systolic function or DCM that allow us to study the interactions between ion channel defects, sympathetic input and myocardial structure. Finally, we also experiment novel pharmacological and peptide- or gene-based therapeutic strategies.
More specifically, our projects for the 2012-2015 period will be to:
1. Elucidate Nav1.5 structure, function, regulation and involvement in arrhythmias and DCM.
2. Investigate the biophysics of ion channels and develop novel peptide-based therapies for arrhythmias.
3. Elucidate the role of b-adrenoceptors deregulation in the pathophysiological mechanisms of heart failure.
4. Engineer bio-artificial pacemakers by gene transfer as a first gene-based therapeutic strategy of cardiac arrhythmias.
5. Generate iPS-derived cardiomyocytes as patient-specific cellular models for investigating the mechanisms of their cardiac arrhythmias and proposing personalized therapies.