The Agoro lab uses systems biology approaches 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 is interested in identifying molecular targets that prevent kidney aging, the progression of chronic kidney disease (CKD), as well as the development of sickle cell nephropathy (SCN). 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 use genetically engineered mouse models, in vitro assays, associated with computational biology tools to study the interplay between iron-driven renal oxidative stress pathways and hormonal signaling in the kidney that are associated with phosphate excretion.
Our ongoing NIH-funded NIDDK R00 Research program is focused on understanding crosstalk mechanisms between renal oxidative stress and FGF23 signaling that mediates phosphate excretion. Currently, in the United States, more than 1 in 7 US adults are estimated to have chronic kidney disease (CKD). CKD is a progressive disease that is associated with loss of important proteins including Klotho (KL), a co-receptor of the bone-derived hormone FGF23 leading to severe endocrine disease, as well as increased renal oxidative stress that further damages the kidneys. The goal of this research program is to identify how the interactions of KL and its ligand FGF23 may contribute to the control of oxidative stress using renal single cell biology approaches. We hope these studies to identify new pathways regulated by FGF23/KL interactions that may be used as novel therapeutic targets to slow down CKD progression.
The second research program in the lab is to identify oxidative stress targets and biological pathways that may contribute to slowing down kidney aging. Our lab aims to isolate key renal redox circuits that drive kidney aging.
The third research program is focused on Sickle Cell Disease. Our team is focused on three specific questions. What are the mechanisms that drive sudden crises in sickle cell disease (SCD) patients? Why do some crises last few hours whereas others take days? What are the biomarkers that predict SCD crises?