Uses systems biology to determine how iron-driven kidney oxidative stress influences FGF23-mediated phosphate excretion in aging, chronic kidney disease and sickle cell anemia.
The Agoro Lab uses Systems Biology approach to identify molecular targets that prevent kidney aging, the progression of chronic kidney disease (CKD), as well as the development of sickle cell nephropathy (SCN). We believe the kidney to be the pioneer organ in mammals, and we are interested in understanding the molecular and cellular dynamics that change in this structurally and functionally complex organ during aging, CKD, and sickle cell anemia. In aged or diseased states, changes in cellular iron metabolism occur in the kidney driving therefore oxidative stress and renal function impairment. One of this function is the decrease of the ability of the kidney to get rid of phosphate from the blood and thus preventing detrimental outcomes such as vascular calcification. Our lab is dedicated to study the mechanisms associated with renal iron handling during physiological and pathological states and how these mechanisms influence the kidney ability to eliminate phosphate from our body. We are using genetically engineered mouse models, in vitro assays, associated with computational biology tools to study the interplay between iron-driven renal oxidative stress pathways and FGF23-mediated phosphate excretion. Understanding the interactions between the above-mentioned biological mechanisms in the kidney is critical for: 1. an optimal physiological performance, 2. an effective interorgan signaling, 3. and a better control of kidney disease progression.