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  • Phone : +33 6 11 09 85 43
  • Location : Toulouse, France

Version françaiseLAURENT MARTINEZ

Last update 2011-12-30 11:01:55.871

LAURENT MARTINEZ PhD, Human Physiopathology.

Course and current status

current laboratory

Director of Research (DR2 INSERM),


Institute of Metabolic and Cardiovascular Diseases (I2MC)

Head of Team 5: "HDL and signaling in atherosclerosis".

CHU Rangueil, BP 84225

31432 Toulouse cedex 04,



Degrees and diplomas

-2007: HDR (Hability to manage Ph.D degree), University of Toulouse III, Paul Sabatier.

-2001: Ph.D in Biochemistry, University of Toulouse III, Paul Sabatier.


Previous laboratories

-2011-Now: Head of Lab at INSERM UMR1048 in Toulouse (Director: Pr. A. Parini), Topic: High Density Lipoprotein (HDL) and signaling in atherosclerosis

-2007-2011: Head of the Avenir group "F1-ATPase in cholesterol metabolism", INSERM U563, Toulouse. Director: Pr. G. Delsol / Pr. B. Perret.

-2004-2010: Researcher (CR INSERM) at INSERM U563 in Toulouse (Director: Pr. G. Delsol), Department of Lipoproteins and Lipid Mediators. Director: Pr. B. Perret.

-2004: Visitor scientist at the Dunn Human Nutrition Unit, Cambridge, United Kingdom. Director: Sir John Walker.

-2001-2003: Postdoctoral fellowship, Columbia University, New-York City, USA. Supervisor: Dr Alan Tall

-1998-2001: PhD student, INSERM U326 (Director: Pr. H. Chap), Toulouse. Supervisor: Dr R. Barbaras


University teatching responsibilities

Since 2005, teaching in master of pathophysiology (2nd year), University of Toulouse III.


Scientific prizes and Awards

 - 2007: Invitation to the 57th meeting of Nobel Laureates at Lindau, Germany.

 - 2007: INSERM “Avenir” Award for the promotion of young researchers.

 - 2005: Invited lecture for the Roche Symposium for Leading Bioscientist of the Next Decade, Basel, Switzerland. March18th, 2005.

 - 2004: Invitation to the 100-year centennial of the ‘Entente Cordiale’ in the presence of Queen Elizabeth and the former French health minister, highlighting the collaboration with the group of J.Walker. Toulouse, France, April 7, 2004.

 - 2003: EMBO visiting fellowship sponsoring scientific collaboration with Dr. J.Walker (Dunn Human Nutrition Unit, Cambridge, UK).

 - 2002: Post-doctoral fellowship “Lavoisier” sponsored by the French government.

Scientific summary

Atherosclerosis is a chronic inflammatory pathogy of the vascular wall, in large part due to the accumulation of macrophages foam cells without adequate removal of cholesterol by High Density Lipoproteins (HDL). Lipid deposits lead to the formation of atherosclerotic plaques that damage the vascular wall and can be further complicated by plaque disruption and thrombosis. Our project is focused on the metabolic and vascular atheroprotective functions of plasma HDL and on phosphoinositide 3-kinase lipid signaling pathways in atherosclerosis and re-stenosis. The project is developed around 3 axes:

         1°) To characterize HDL-mediated Reverse Cholesterol Transport (RCT).

The protective effect of HDL against atherosclerosis is mostly attributed to their central functions in RCT. In this context, we identified a metabolic sequence in which apolipoprotein A-I (apoA-I) binds to ATP-synthase (F1-ATPase) at the surface of hepatocytes, triggering ATP hydrolysis. The generated ADP interacts with the P2Y13 receptor, which in turn stimulates HDL uptake. We currently evaluate the physiological relevance of this HDL-uptake pathway in atherosclerosis and its regulation.

         2°) To characterize new signaling pathways and therapeutic approaches in vascular wall protection.

We have previously demonstrated that the gamma isoform of PI3K plays an essential role in inflammatory processes of vascular wall in atherogenesis. We now propose to study PI3K and apoA-I induced-signaling pathway in arterial wall to define these two pathways as new therapeutic approaches to prevent vascular dammages.

         3°) Determinants of HDL levels and functions and cardiovascular risk.

         We investigate genotypic or biological factors associated with HDL levels in the general population, in patients with coronary artery diseases and in patients exposed to an increased risk of dysmetabolic syndrome.

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