In osteoarthritis, articular cartilage undergoes progressive degradation in which low-grade inflammation may play a central role, in particular through a mechanism related to oxidative stress, exposure to reactive oxygen species (ROS) and alterations in chondrocyte metabolism. We have shown in vivo that ROS production by chondrocytes via NADPH isoform 4 (NOX4) plays a detrimental role in the pathogenesis of osteoarthritis. Our research focuses on the regulatory mechanisms of osteoarthritis pathophysiology by NOX4. First, we are investigating the impact of synovial inflammation in osteoarthritis and the role of NOX4 in its regulation. Secondly, we will investigate the changes in chondrocyte metabolism in osteoarthritis and the dependence of these changes on NOX4. We are particularly interested in the role of the switch between glycolysis and the Krebs cycle, as well as lipid beta-oxidation.

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