Mechanistic study on the pathogenic role of cell division autoantigen 1 in diabetic kidney disease in Akita mice

This thesis focuses on diabetic kidney disease, a major complication of diabetes that can lead to kidney failure. I investigate the role of the CDA1 protein in driving kidney fibrosis, a common pathological feature of diabetic kidney disease that damages kidney structure and function. By removing this protein in a diabetic mouse model, kidney fibrosis and injury are noticeably reduced. These findings suggest that blocking the activity of CDA1 could help slow or prevent kidney damage. This research provides new insight into diabetic kidney disease and highlights CDA1 as a promising target for future therapies.