New therapeutic strategy for diabetic nephropathy via autophagy regulation

2015 Fiscal Year Final Research Report

• Project/Area Number: 25670414
• Research Category: Grant-in-Aid for Challenging Exploratory Research
• Allocation Type: Multi-year Fund
• Research Field: Kidney internal medicine
• Research Institution: Kanazawa Medical University
• Principal Investigator: KOYA Daisuke 金沢医科大学, 医学部, 教授 (70242980)
• Co-Investigator(Kenkyū-buntansha): KANASAKI Keizo 金沢医科大学, 医学部, 准教授 (60589919) ; KANASAKI Megumi 金沢医科大学, 医学部, 助教 (50599355)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: オートファジー / 糖尿病 / 内皮・間葉転化 / microRNA

Outline of Final Research Achievements

Renal fibrosis in diabetic mouse model was ameliorated by inhibition of endothelial-mesenchymal conversion via the anti-fibrotic microRNA29 and let-7 induction with an endogenous anti-fibrotic peptide N-acetyl-seryl-aspartyl-lysyl-proline (AcSDKP) administration. In addition, although renal fibrosis has been caused by the enhancement of the DPP-4 expression by reduced microRNA29 expression in diabetic state, it has improved by microRNA29 expression with a DPP-4 inhibitor, linagliptin administration.

Free Research Field

医歯薬学