Our group investigates how redox metabolism and reactive oxygen species (ROS) govern cellular adaptation in health and disease, with a focus on pancreatic β-cells, metabolic disorders, and cardio-renal complications. We combine advanced redox imaging, metabolic physiology, and disease models to understand how compartment-specific H2O2 production and redox signaling determine cell fate, function, and stress responses.
Our work bridges redox biochemistry, metabolism, and physiology, emphasizing H₂O₂ as a central regulator of metabolic adaptation. We study how NADPH/NADP⁺ balance, NOX activity, and localized ROS shape signaling networks controlling metabolism, stress resistance, and survival. In β-cells, physiological H2O2 fluctuations fine-tune insulin secretion, whereas excessive or NOX2-derived H2O2 drives dysfunction under lipotoxic or inflammatory stress. Similar principles extend to cardiac and renal cells, where H2O2 mediates adaptive and maladaptive signaling that influences mitochondrial function, calcium handling, and inter-organ crosstalk.
To dissect these mechanisms, we have developed a comprehensive toolbox for quantitative, compartment-resolved redox biology, including genetically encoded biosensors (HyPer7, NAPstar, roGFP2-Orp1, GRX1-roGFP2) and chemogenetic H2O2-generation systems. These tools enable real-time visualization and causal testing of redox dynamics in living cells and tissues. Combined with our redox histology approach for fixed samples, they provide unprecedented insight into how spatially and temporally defined redox changes regulate metabolism, calcium signaling, and gene expression across tissues.
