We study all aspects of human podocyte disease (also termed “podocytopathy”). Podocyte is a cool epithelial cell essential for the filtering function of the kidney. Podocytopathy often leads to proteinuria and glomerulosclerosis, a major pathology of chronic kidney disease.

Using advanced transcriptome, molecular cloning, microscopic imaging and basic science approaches in both cell and animal models of podocytopathy, we try to understand the molecular events underlying the pathogenesis of podocytopathy to direct a rational development of novel therapies.

Our primary research aims at dissecting the molecular disturbance in protein trafficking pathways mediated by dynein motor protein complex as potential therapeutic targets for both genetic and acquired podocytopathy like diabetic podocytopathy. We use multidisciplinary approaches to characterize dynein-driven pathogenesis of podocytopathy caused by mutations in INF2 gene, as well as diabetic podocytopathy. Our approaches include classic molecular and cellular biology tools, live cell imaging and quantitative analysis of trafficking dynamics using mathematical models, podocyte cell lines with CRISPR-facilitated gene editing, podocyte-specific dynein transgenic mice in combination with Type I and Type II diabetes models.

The second project is to investigate the personalized spatial transcription profile of human podocytopathy of different etiologies, using the cutting-edge methodology of Visium spatial transcriptomics. Collaborating with the NeuroBank Core, the Genomics Division of the Iowa Institute of Human Genetics and the Bioinformatics Core, we aim to identify the transcriptome-clinicohistological correlations, dissect pathological pathways to direct a personalized precision diagnosis and treatment for each individual patient with podocytopathy.