Professor | YOKOI Hideki |
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Associate Professor | KUWABARA Takashige ktakasea(at mark)kumamoto-u.ac.jp |
Assistant Professor | MIZUMOTO Teruhiko tmizumoto(at mark)kumamoto-u.ac.jp |
Assistant Professor | FUJIMOTO Daisuke dfleppard1002(at mark)kumamoto-u.ac.jp |
Our research focuses on kidney damage associated with hypertension and diabetes, particularly investigating podocyte injury and inflammatory responses. It has been found that the receptor for natriuretic peptides, GC-A, is expressed in podocytes, and GC-A-deficient mice exhibit aggravated glomerular injury upon aldosterone stimulation. Detailed studies are underway to elucidate this mechanism. In lifestyle-related kidney diseases such as diabetic nephropathy, inflammatory signals including TLR4 and its ligand MRP8 play a key role, and we aim to develop therapies targeting these molecules. Furthermore, single-cell analysis of glomeruli from diabetic model mice has identified new candidate molecules related to glucose metabolism and inflammation, and their functional roles are under investigation. The transcription factor NFAT5, expressed in tubular cells, is involved in urine concentration and salt-sensitive hypertension, suggesting a potential therapeutic target in chronic kidney disease. We are also exploring the molecular basis of sodium metabolism regulation via ENaC and serine proteases, aiming to develop novel antihypertensive treatments. In the field of dialysis, we are studying mechanisms of peritoneal damage in long-term peritoneal dialysis, focusing on factors such as CTGF and MMP-10, to achieve extending dialysis period through innovative therapies.