Investigating a new therapeutic approach from autophagy-deficient associated protein

2014 Fiscal Year Final Research Report

• Project/Area Number: 24659416
• Research Category: Grant-in-Aid for Challenging Exploratory Research
• Allocation Type: Multi-year Fund
• Research Field: Kidney internal medicine
• Research Institution: Osaka University
• Principal Investigator: ISAKA Yoshitaka 大阪大学, 医学(系)研究科(研究院), 准教授 (00379166)
• Co-Investigator(Kenkyū-buntansha): TAKABATAKE Yoshitsugu 大阪大学, 大学院医学系研究科, 助教 (30403075)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: 腎臓内科学 / オートファジー / 尿細管傷害 / 活性酸素 / ミトコンドリア / リソソーム / 酸化ストレス / 急性腎障害

Outline of Final Research Achievements

Macroautophagy is a highly evolutionally concerved degradation process by which cytosolic materials and damaged organelles are broken down to their basic component. We investigated the role of autophagy in proximal tubular epithelial cells using autophagy- deficient mice and cultured tubular cells. Autphagy guarded proximal tubular cells against kidney injury by cisplatin, cyclosporine, urate crystal, or metabolic acidosis. The protective mechanism is to alleviate DNA damage, reactive oxygen species by eliminating damaged mitochondria, ruptured lysosomes, or aggregated protein. In addition, autophagy acts to ameliorate the chronic metabolic stress induced by cyclosporine or metabolic acidosis. These data provide new therapeutic perspective in chronic kidney diseases.

Free Research Field

腎臓内科学