The main focuses of our lab is elucidating the molecular mechanisms that contribute to the development of proteinuria in glomerular diseases of metabolic and non-metabolic origin with an emphasis on podocyte injury induced by disordered lipid metabolism. Our lab employs discoveries made in the lab to develop therapeutics in the Katz Family Drug Discovery Center.

Currently we are focusing on the following areas to drive discovery:

• Defining the role of stimulator of interferon genes (STING) in the development and progression of diabetic kidney disease and focal segmental glomerulosclerosis using various mouse models of DKD and FSGS. Understanding of the molecular mechanisms leading to STING constitutive activation and chronic sterile inflammation will open new therapeutic opportunities to treat glomerular diseases.
• Understanding the intricate interplay of the lipid trafficking protein OSBPL7 and cellular metabolism, elucidating its multifaceted role in autophagy, lipid regulation, ER stress, and podocyte injury, particularly within the context of Chronic Kidney Disease. By employing diverse models, including mice and zebrafish, alongside in vitro methods, our team has identified a relationship between OSBPL7 deficiency and various cellular functions. 
• Exploring fatty acid metabolism, lipid droplet and mitochondria communication, and the cellular responses to different matrix environments in the progression of Alport Syndrome
• Identifying a novel mechanism linking Perilipin 5 (PLIN5) deficiency to lipotoxicity-mediated podocyte injury in Alport Syndrome (AS). Our hypothesis suggests that PLIN5 deficiency in AS causes increased triglyceride lipolysis and impaired chaperone mediated autophagy (CMA)-mediated LD breakdown, resulting in lipotoxicity-induced mitochondrial dysfunction and podocyte injury.
• Studying a dysregulation of components in the Apolipoprotein M and Sphingosine-1-phosphate pathways in multiple disease modalities.