Isabelle Passagne
  • E-mail :[email]
  • Phone : 33557571010
  • Location : Bordeaux, France
Last update 2020-05-29 12:14:42.603

Isabelle Passagne Associate professor (MCU) fn university of Bordeaux, PhD in Toxicology, PharmD

Course and current status

Present address:

UMR1034 Inserm / University of Bordeaux

Biology of Cardiovascular Diseases1 avenue de Magellan –33604 Pessac
Phone : 05 57 89 19 79



  • Since 2018 : Member of CROP (Conseil régional de l'Ordre des pharmaciens)
  • Since 2006 : Associate Professor (MCU)  in Toxicology ; University of Bordeaux
  • Nov. 2004-2006 :  Assistant Lecturer/Researcher (ATER)  in the Laboratory of Hydrology –Environment ; University of Bordeaux
  • Oct. 2004 : Ph.D. in Toxicology; University of Montpellier
  • 2001 : Master’s degree in Toxicology ; University Paris VII
  • 1999 : Doctor in Pharmacy ; University of Aix-MArseille

Scientific summary

Impairment of blood vessels in the retinal vasculature, has been implicated in several human diseases, including retinopathy of prematurity and diabetic retinopathy. Recent studies have shown an association between diabetic retinopathy and premature senescence. In fact, early microvascular changes was associated to vascular permeability and defective vascular repair. The vascular changes have been linked to increased formation of reactive oxygen species (ROS) and decreased formation of NO, which has function as a vasodilator and anti-inflammatory factor. This can cause premature endothelial cell senescence with the involvement of NADPH oxidases. Limiting the actions of NADPH-oxidase could provide a new strategy for treating. Accordingly, when we investigate the pathogenesis of human vascular diseases, it may be more important to answer the question of how age specifically promotes it. Our laboratory want to answer at this question. In fact, molecular mechanisms by aging remain unclear. Our laboratory can develop an In vitro model for evaluating the effect of aging on human endothelial cells and studying molecular signaling of oxidative stress, implicated in aging- dependent retinopathy.

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