Our lab is interested in identifying molecular targets that prevent kidney aging, the progression of chronic kidney disease, as well as the development of sickle cell nephropathy. In aged or diseased states, changes in cellular iron metabolism occur in the kidney driving therefore oxidative stress and renal function impairment.
One of our projects is focused on understanding crosstalk mechanisms between renal oxidative stress and FGF23 signaling that mediates phosphate excretion. We are also working to identify oxidative stress targets and biological pathways that may contribute to slowing down kidney aging.
Lastly, we are working on sickle cell disease (SCD). We are interested in identifying the mechanisms that drive sudden crises in SCD patients, what influences the duration of the crises and what biomarkers predict SCD crises.