Members

My major area of research interest include the endocytic process and matrix regulation in podocytes. Our laboratory has identified the critical role of the clathrin coated endocytic processes in the development and maintenance of podocytes. In-vivo animal models with conventional or conditional ablation of genes implicated for endocytosis, such as synaptojanin, endophilin, and dynamin develop severe proteinuria and foot process effacement. By utilizing fluorescently tagged proteins, we have visualized these proteins along with genes implicated to cause human nephrotic syndrome (CD2AP, Myo1e, Nephrin) lie at the interface of endocytosis and actin cytoskeleton. One of the major goals of the laboratory is investigating and further understanding the critical factors that are being endocytosed in podocytes. We have also sought to examine the role of cell matrix interactions by providing mechanistic insight on focal adhesion proteins and integrins, which govern podocyte cell adhesion and movement during health and disease states, using mouse genetic models of disease.

My current research project revolves around studying mechanisms that regulate cytoskeletal dynamics and their roles in podocyte function and dysfunction. In addition, I am also interested in defining potential subpopulations of podocytes by leveraging computational methods and published single-cell RNA-seq datasets. As a physician scientist in training, my big picture goal is to identify novel therapeutic targets that can be used to specifically address podocyte dysfunction in people with CKD.

My research interests include mechanisms of autoimmune glomerular disease (membranous nephropathy, minimal change disease), and dissecting the role of specific calpain system isoforms in mediating podocyte injury. Clinically, I am interested in diagnostic medical renal pathology, genitourinary pathology, and the assessment of chronic kidney disease at autopsy.

My research interest is to study podocyte senescence as an important cause of podocyte loss and chronic kidney diseases. I am particularly interested in 1) identifying the mechanisms that podocytes use to repair DNA damage and prevent senescence from occurring, 2) elucidating the mechanisms by which podocyte senescence can lead to kidney failure.

My research interest is to study the mechanism ongoing mechanisms of APOL1 disease where risk alleles G1 and G2 results in a higher rate of chronic kidney disease in patients of African Ancestory. We will leverage using BAC transgenic mice that express human APOL1.

Persistent proteinuria is one of the critical independent risk factors resulting into end-stage kidney disease. My primary interest lies in identifying the mechanisms of how podocyte injury results in the loss of integrity of the kidney filtration barrier and it can be potentially translated from the bench to bedside.