Regulation of mitochondrial function for protection of acute kidney

2016 Fiscal Year Final Research Report

• Project/Area Number: 15K15331
• Research Category: Grant-in-Aid for Challenging Exploratory Research
• Allocation Type: Multi-year Fund
• Research Field: Kidney internal medicine
• Research Institution: Kochi University
• Principal Investigator: TERADA Yoshio 高知大学, 教育研究部医療学系臨床医学部門, 教授 (30251531)
• Project Period (FY): 2015-04-01 – 2017-03-31
• Keywords: 尿細管 / 腎不全 / オートファジー / マイトファジー

Outline of Final Research Achievements

Acute kidney injury (AKI), often resulting from ischemic, toxic, and septic insults, is a common disorder with a high morbidity and mortality. The major morphologic changes in ischemic AKI include the effacement and loss of the proximal tubule brush border, patchy loss of tubular cells, areas of focal proximal tubular dilation, apoptosis, necrosis, and inflammation. We showed that HSPB1 expression increased　during oxidative stress in AKI. Incremental　HSPB1 expression increased autophagic flux and inhibited apoptosis in renal tubular cells. These results indicate that HSPB1 upregulation plays a role in the pathophysiology of AKI.

Free Research Field

腎臓内科