The overall goals of my research are to define the role of podocyte endoplasmic reticulum (ER) stress in the pathogenesis of nephrotic syndrome (NS) and to investigate potential therapies. NS is an important kidney disease, which causes heavy proteinuria, hypoalbuminemia, hyperlipidemia, and increased risk of progressive loss of kidney function. However, there is no effective treatment for most cases of NS associated with genetic mutations. We are utilizing a combination of stably transfected cell lines, transgenic and knockout animal models, and NS patient samples. The integrated approach enables us to delineate the podocyte ER stress signaling cascades, to identify novel biomarkers, and to investigate mechanism-based therapies.

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