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Hideki Kato, M.D., Ph.D.
Post-Doctoral Fellow
After he graduated my medical school of Tokyo University in Japan in 1998, Hideki Kato, M.D., Ph.D. decided to specialize in nephrology since nephrology seemed the most exciting and the most difficult specialty in medicine. During his residency and fellowship trainings, he saw many patients with nephrotic syndrome and renal failure. However, unfortunately he could not offer any specific treatment for these patients. This critical experience led me to study the mechanism of proteinuria and renal failure with a special emphasis that Kato would like to develop new treatment modalities for this disease.
Bronx, New York
Albert Einstein College of Medicine
Lay Summary of the Project:
The mechanism of FSGS is still unknown. Recent studies indicate that podocyte in the glomeruli play a pivotal role in glomerular sclerosis development. We found that genes that belong to wnt/β-catenin signaling are regulated in podocytes in humans and mouse models of glomerular injury. Wnt/β-catenin signaling pathway has been considered to play important role for the kidney developemnt and to regulate gene expression and maintain cell interaction. However its role in disease condition is unknown. In order to examine the role of β-catenin signaling in podocyte, we generated the mice which overexpress and lack β-catenin specifically in podocyte. Our studies indicate that overexpression of β-catenin in podocytes led to the development proteinuria and glomerulosclerosis similar to FSGS and deletion of β-catenin in podocytes showed increased susceptibility for proteinuria. My goal is to understand the role of β-catenin in glomerulosclerosis, proteinuria and FSGS. This reseach can lead to the development of better diagnostics and also potentially to new treatments for glomerulosclerosis and FSGS.
