Kidney podocytes are the target cells for injury in human glomerular disease, a significant cause of end stage kidney failure. Primary and secondary pathogenic processes affecting podocytes account for 90% of end-stage kidney disease at a cost of 20 billion dollars per year in the US. A reduction in podocyte number (podocytopenia) directly correlates with the progression of several proteinuric kidney diseases including focal segmental glomerulosclerosis (FSGS), IgA nephropathy and diabetic nephropathy. Despite significant advances in the characterization of the molecular architecture of podocytes, the mechanisms underlying their survival, injury and loss remain poorly understood. Validated therapeutic targets are scarce and there are currently no podocyte-specific drugs commercially available. The overall goal of our research program is to enhance the pipeline of putative therapeutic targets available to tackle human glomerular disease by elucidating the details and functional significance of key signaling pathways that regulate podocyte injury and survival. We utilize cell-based assays and rodent models to identify and characterize key mediators of glomerular disease progression.