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Given the acknowledged role of reactive oxygen species and electrophilic lipids derived from LDL oxidation in the development of atherosclerotic lesions, the interest of our laboratory has been to elucidate the effect of Nrf2 on the atherogenic process. To this end, we have employed a number of in vitro methods to study relevant cell types (e.g. endothelial cell cultures both from human and mice, mouse peritoneal and bone marrow derived macrophages) and in vivo mouse models of atherosclerosis (bone marrow transfer to Ldlr-/- mice, Nrf2 deficient mice in Ldlr-/- and Ldlr-/-ApoB100/100 background). We will discuss our recent findings utilizing these models and limitations they may have. In addition, we showcase our novel models to better recapitulate the tissue-specific role of Nrf2 in cardiometabolic diseases (endothelium and liver specific Nrf2 deficient mice in combination with Ldlr-/- deficiency/AAV-mediated delivery of mutant PCSK9). These models are useful for preclinical studies assessing the vascular and metabolic effects of Nrf2 modulating drugs.