PRESENT POSITION
Director of Research INSERM
Deputy Director of the Institute of Cardiovascular and Metabolic Disease,
INSERM-University of Toulouse, France
Head of the Laboratory, "Signaling and Pathophysiology of Heart failure"
INSERM UMR-1297
University of Toulouse
EDUCATION
2000 Accreditation to direct research, Speciality: Pharmacy, University of Paris-Saclay
1995 Ph.D in Molecular Endocrinology, with Honors, University Pierre & Marie Curie, CNRS-Museum National d’Histoire Naturelle, Paris
1991 Master Degree in Molecular Endocrinology, University of Paris-Saclay
APPOINTMENTS
2021- Research Director (DR1) INSERM
2018 Deputy Director of I2MC, INSERM, University of Toulouse
2014 Head of the department « Cardiac & Kidney Remodeling», INSERM, University of Toulouse
2011 Head of Laboratory « Signaling & Pathophysiology of Heart Failure», INSERM, Toulouse
2006-10 Team leader « Small G protein and Cardiac Pathophysiology», INSERM UMR-769, Faculty of Pharmacy, University of Paris-Sud, Châtenay-Malabry, France
2005-20 Research Director (DR2) INSERM
1999-05 Group leader «Molecular and Pharmacological Characterisation of 5-HT4 receptors», INSERM U-446, Faculty of Pharmacy, University Paris-Sud, Châtenay-Malabry, France
1999 Research Associate (CR1) INSERM “Cellular & Molecular Cardiology”, University of Paris-Sud, Châtenay-Malabry, France
1998 Postdoc, INSERM “Cellular & Molecular Cardiology”, University of Paris-Sud, Châtenay-Malabry, France
1996-97 Postdoc, Max-Planck-Institute für Psychiatrie, Neuroendocrinology, Munich,
HONOURS and AWARDS
Memberships and involvement in organizations
PUBLICATIONS
VALORISATION
INVITED TALKS
- International Society for Heart Research (2021, 2019, 2018, 2017, 2015)
- European Society of Cardiology (2019, 2017), Gordon Conf. USA (2015)
MENTORING
AREA of RESEARCH
MECHANISMS of HEART FAILURE - THERAPEUTICS INNOVATION - CARDIOVASCULAR DISEASE - SIGNALING - METABOLISM
Heart failure (HF) is among the most prevalent diseases in developed countries and its incidence tends to increase dramatically with aging. We aim to determine specific intracellular signaling networks activated by acute or chronic cardiac stress (ischemia, adrenergic overdrive) with the overarching objective of identifying relevant drug targets to treat or block the progression of HF.
We have characterized novel signalosomes involved in cardiac pathological remodeling (hypertrophy, fibrosis, cell death) in response to adrenergic over-stimulation and ischemia (acute or chronic). These signaling events occur in different subcellular compartments (i.e mitochondria) and mainly involve the cAMP-binding protein Epac1. In addition, we have also identified a novel protein named Carabin and an Epac1 pharmacological inhibitor (AM-001) that protect the heart against cardiac stress and prevent the development of HF. Our research project is a follow up of the work done by the team over the past three years:
1- Decipher how non-classical signaling proteins (i.e Epac, Carabin) located in subcellular compartments (i.e nucleus, mitochondria) influence key cellular processes (i.e metabolism, death, hypertrophy) and contribute to the development of HF, including HF with preserved ejection fraction (HFpEF).
2- Decode the molecular and cellular mechanisms involved in cardiomyocyte senescence and cardiac ageing and study their impact in age-associated cardiac diseases including HFpEF.
3- Develop therapies for cardiac disease based on new knowledge derived from our studies.