Research Project
Grant-in-Aid for Challenging Exploratory Research
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.
All 2017 2016 2015
All Journal Article (5 results) (of which Peer Reviewed: 2 results, Open Access: 1 results) Presentation (4 results) (of which Int'l Joint Research: 1 results) Book (2 results)
Clin Exp Nephrol.
Volume: 20 Issue: 6 Pages: 827-831
10.1007/s10157-016-1334-0
120007135282
Clin. Exp. Nephrol.
Volume: 印刷中 Issue: 6 Pages: 918-925
10.1007/s10157-016-1231-6
日本腎臓学会誌
Volume: 58 Pages: 31-34
Volume: 58 Pages: 1079-1082
40021008317
PLOS one
Volume: 10 Issue: 5 Pages: e0126229-e0126229
10.1371/journal.pone.0126229