Team members

Nègre-Salvayre
Anne
(DR1)

Nègre-Salvayre Anne (DR1)

anne.negre-salvayre@inserm.fr

33(0)561322059




Present position
- DR1 CNRS
- Team leader: Lipid peroxidation and signaling in vascular diseases
- Deputy director INSERM U1048 - Institute of Metabolic and Cardiovascular Diseases

University degrees
- Pharmacist Toulouse 1976
- Graduated in Clinical Biology Toulouse 1980
- Doctorate in Pharmaceutical Sciences - Toulouse 1983
- PhD (Human Biology) - Toulouse 1987
- Research Supervisor - Toulouse 1992

Scientific career
1983-1988 Post-doctoral fellow, Hadassah Medical School Jerusalem, Israel
1985-2001: Established investigator (CR2 and CR1) INSERM U101 and INSERM U466 Toulouse
2001-2009: Senior researcher (Directeur de Recherche) CNRS DR2
2009-running: Senior researcher (Directeur de Recherche) CNRS DR1
2007-2010: Head of Team 10 "Atherosclerosis and graft arteriosclerosis", INSERM U858 - Toulouse
2011-2015: Head of Team 10 "Atherosclerosis and graft arteriosclerosis", INSERM UMR1048 - Toulouse
Running: Head of the Team10 "Lipid Peroxidation and signaling in Vascular Diseases", INSERM U 1048
Since 2016: Deputy director INSERM U1048

Hospital duties
1978-1985: Fellow and Instructor, Medical Biochemistry Laboratory, CHU Purpan Toulouse

Teaching and Training
1982-1983: Assistant Professor in Medical Physiology, Faculty of Medicine Rangueil, Toulouse
1981-1982: Instructor, Biochemistry Department, Faculty of Medicine Purpan, Toulouse
1974-1976: Instructor, Biochemistry Department, Faculty of Pharmacy, Toulouse

Scientific activities and expertise
Membership of learned societies: New Society for French Atherosclerosis (NSFA), Society for Free Radical Diseases (SFRR), HNE-Club, Oxygen Club of california (OCC), British Pharmacological Society

Associate Editor "The British Journal of Pharmacology"
Vindis
Cécile
(DR2)

Vindis Cécile (DR2)

cecile.vindis@inserm.fr

33(0)561322705

Augé
Nathalie
(CR1)

Augé Nathalie (CR1)

nathalie.auge@inserm.fr

33(0)561323421

Bernis
Corinne
(TR)

Bernis Corinne (TR)

corinne.bernis@inserm.fr

33(0)561323421

Bonneville
Jonathan
(Doc)

Bonneville Jonathan (Doc)

jonathan.bonneville@inserm.fr

33(0)561323391

Camaré
Caroline
(AHU)

Camaré Caroline (AHU)

caroline.camare@inserm.fr

33(0)561322061

Faccini
Julien
(IE-CDD)

Faccini Julien (IE-CDD)

julien.faccini@inserm.fr

33(0)561322705

Geoffre
Nancy
(AJT 50%)

Geoffre Nancy (AJT 50%)

nancy.geoffre@inserm.fr

33(0)561323421

Guerby
Paul
(Doc)

Guerby Paul (Doc)

paul.guerby@inserm.fr

33(0)561323510

Ingueneau
Cécile
(MCU-PH)

Ingueneau Cécile (MCU-PH)

ingueneau.c@chu-toulouse.fr

33(0)561323447

Meyer
Elbaz
(PU-PH)

Meyer Elbaz (PU-PH)

elbaz.m@chu-toulouse.fr

33(0)561322705

Meyrignac
Olivier
(PH)

Meyrignac Olivier (PH)

meyrignac.o@chu-toulouse.fr

Moreno
Ramiro
(IR-CDD)

Moreno Ramiro (IR-CDD)

ramiro.moreno@inserm.fr

Moulis
Manon
(Post-Doc)

Moulis Manon (Post-Doc)

manon.moulis@inserm.fr

33(0)561323391

Nahapetyan
Hripsimé
(Doc)

Nahapetyan Hripsimé (Doc)

hripsime.nahapetyan@inserm.fr

33(0)561322705

Rouahi
Myriam
(IE)

Rouahi Myriam (IE)

myriam.rouahi@inserm.fr

33(0)561322061

Rousseau
Hervé
(PU-PH)

Rousseau Hervé (PU-PH)

rousseau.h@chu-toulouse.fr

Salvayre
Robert
(PU-PH EM)

Salvayre Robert (PU-PH EM)

robert.salvayre@inserm.fr

33(0)562323148

Santiago
Christophe
(AJT 50%)

Santiago Christophe (AJT 50%)

christophe.santiago@inserm.fr

33(0)561323421

Sewonu
Anou
(IR-CDD)

Sewonu Anou (IR-CDD)

kwadzo.sewonu@inserm.fr

Swiader
Audrey
(AI)

Swiader Audrey (AI)

audrey.swiader@inserm.fr

33(0)561323510

Low density lipoproteins (LDL)'s modifications in the vascular wall, by oxidation, glycation, glycoxidation or aggregation, plays a key-role in the early stages of atherogenesis, characterized by the accumulation of foam cells, the formation of fatty streaks and the proinflammatory immune response.

During the progression of atherosclerosis, oxidized lipids accumulate in the necrotico-lipid core, and participate in the development of lesions towards more advanced stages. Oxidized lipids promote local inflammatory responses, stimulate the migration and proliferation of smooth muscle cells, as well as the extracellular matrix production and plaque remodeling. These lipids are involved in angiogenesis, induce apoptosis and contribute to vascular aging. Oxidized lipid properties depend on their local concentration, their nature (oxidized phospholipids, oxysterols, aldehydes…), their uptake by scavenger receptors (CD36, LOX-1, SRA...) that differ as function of the cell type. Finally, oxidized lipids can generate cellular responses (oxidative stress, protease secretion, cellular dysfunction, apoptosis ...), which contribute to fragilize the lesions, promote plaque erosion or rupture and finally lead to athero-thrombosis events.

Our team "Lipids, Peroxidation, Signaling in Vascular Diseases" involves researchers, clinicians and technicians aiming at better understanding the mechanisms involved in plaque progression and instability, and particularly the factors related to LDL modification and oxidation. In our previous studies, we have deciphered some atherogenic properties of oxidized LDL and lipids, such as the mechanisms implicated in the balance between cell survival and death, that conditions the fate of vascular cells. These pathways include the ceramide/sphingosine-1-phosphate rheostat, which promotes the survival, migration and proliferation of smooth muscle cells, and constitutes a key mechanism (with VEGF) for the development of neoangiogenesis, the endoplasmic reticulum stress implicated in cell survival and apoptosis, the cytosolic calcium dysregulation, which plays an essential role in cell death induced by oxidized LDL, the presence of antioxidant and antiapoptotic defense systems, or the autophagy and mitophagic pathways involved in survival and efferocytosis. The modification of cellular proteins by aldehydes generated during lipid peroxidation, progressively alters these protective functions and contributes to cellular dysfunction and apoptosis.

Our objectives are to i / identify and characterize the role of oxidized lipids and modified LDL in the progression of atherosclerotic lesions, and more precisely the mechanisms of neoangiogenesis, vascular aging, calcification of advanced plaques, or the protective role of autophagy and mitophagy in the fate of the plaque (ii) developing innovative computational vascular medical imaging techniques for visualizing vascular hemodynamics and wall shear stress, and (iii) identifying new non-invasive biomarkers for the coronary patient follow-up.