CV Science

Cécile Vindis PhD in Molecular and Cellular Pharmacology

Course and current status

Professional address: INSERM, UMR-1048, Institute for Cardiovascular and Metabolic Diseases, F-31342 Toulouse, France. Director A. Parini

Present position: Research Director (DR2, HDR) at INSERM, team “Lipids, Peroxidation, Signaling and Vascular Diseases”, INSERM, UMR-1048/I2MC

 EDUCATION

2005- Diploma in Animal Experimentation, National Veterinary School of Toulouse.

2000- Ph.D in Molecular and Cellular Pharmacology, University Paul Sabatier, Toulouse. Fellowship awarded by the French Ministry of Education and Research. INSERM U388, Molecular Pharmacology and Renal Physiopathology, Toulouse (Director  A. Parini).

1996- Master Degree 2  Molecular and Cellular Pharmacology, University Paul Sabatier Toulouse

1995- Master Degree 1  Biochemistry, Biological Chemistry and Biophysics, University Paul Sabatier, Toulouse

 RESEARCH EXPERIENCE

2005-at present INSERM Senior Researcher, INSERM, UMR-1048, Institute for Cardiovascular and Metabolic Diseases. Research topics : Cellular and molecular mechanisms involved in the cell survival/death balance of vascular cells - Role in vascular remodeling and atherogenesis

2003-2005  Post-doctoral Fellow, INSERM U-466 (Dir. R.Salvayre), Toulouse. Post-doctoral fellowship awarded by INSERM (Contrat de recherche jeunes chercheurs).

2000-2003  Post-doctoral Fellow, Department of Nephrology and Clinical Research, University of Bern, Switzerland              

Scientific summary

• Investigating the cellular and molecular mechanisms involved in the cell survival (ER stress, autophagy/mitophagy) and death (apoptosis, necrosis) balance during atherogenesis
• Looking at  the role of atherogenic factors: oxidized lipoproteins and oxidized lipids in triggering cell survival and death signaling pathways.
• Investigating the mechanisms involved in the protective role of HDL. Evaluating the qualitative and functional properties of HDL in patients with coronary artery disease.

These studies use a combination of cell models (vascular cells and macrophages), mouse models of atherosclerosis, human atherosclerotic plaques and human clinical data.