Pinelopi Kapitsinou, MD, is a physician-scientist focused on how oxygen sensing rewires metabolism and inflammation in kidney disease. Her lab has dissected isoform-specific roles of endothelial prolyl hydroxylases (PHDs). Early work showed that endothelial PHD2 inhibition activates HIF-2 and causes pulmonary hypertension. Turning to the kidney, her team then uncovered a previously unrecognized metabolic program: endothelial PHD loss rewires glycolysis in the injured kidney, induces the lactate transporter MCT4, and drives inflammation and fibrosis. This kidney-specific metabolic switch marks a checkpoint in repair, and it is druggable, as MCT4 inhibition restores adaptive repair. Complementing these vascular mechanisms, Dr. Kapitsinou's lab discovered that the IDO1–kynurenine–NAD⁺ axis connects hypoxic preconditioning and pharmacologic PHD inhibition to kidney protection, establishing tryptophan metabolism as a pathway of tissue resilience. Her lab is currently investigating endothelial metabolism and pseudohypoxia in post-ischemic repair, defining immune-metabolic mechanisms of kidney repair, and mapping compartment-specific NAD metabolism across the AKI-to-CKD continuum. Dr. Kapitsinou's research program aims to pinpoint actionable nodes and biomarkers to guide new therapies for acute and chronic kidney disease.