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Cardiovascular diseases still remain the major cause of morbidity and mortality worldwide due to the growing prevalence of obesity and associated metabolic disorders, including insulin resistance and Type 2 diabetes. Dyslipidemia, characterized by altered circulating concentrations of lipoproteins and lipids is a major component in the development of cardiometabolic diseases (CMD). As a consequence, lipid-lowering therapies are the privileged therapeutic strategy in CMD. Mechanisms through which lipids contribute to the development of metabolic disorders are multiple and involve complex signaling and regulation pathways at the both cellular and systemic levels. Importantly, it is now clear that a large spectrum of lipid species not only restricted to cholesterol and triglycerides participates actively in alterations of lipid and lipoprotein metabolism in CMD. Then, deciphering of dysfunctional lipid metabolic pathways might help to propose new therapeutic targets to prevent or hamper the occurrence and development of CMD.
Our recent pioneering studies leading to the identification by omics approaches of lipid networks and metabolic pathways controlling biological activities of plasma lipoproteins and cell activation in CMD open up new insights in understanding how alterations in lipid metabolism contribute to CMD onset. In particular, our recent findings lead us to revisit the current understanding of atheroprotective high-density lipoprotein (HDL) and triglyceride-rich lipoprotein (TRL) metabolism and its role in CVD.
Building on tight interactions with clinical and valorization departments, our research program aims to propose new candidate pathways, genes and biomarkers in the context of CMD.
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