Curcumin alleviates ischemia reperfusion‐induced late kidney fibrosis through the APPL1/Akt signaling pathway
As a major cause of renal failure, transient renal ischemia and reperfusion induce both acute kidney injury and late fibrosis, which are the common pathological manifestations of end‐stage renal disease. Curcumin is a biologically active polyphenolic compound found in turmeric. Increasing evidence h...
Saved in:
Published in | Journal of cellular physiology Vol. 233; no. 11; pp. 8588 - 8596 |
---|---|
Main Authors | , , , , , |
Format | Journal Article |
Language | English |
Published |
United States
Wiley Subscription Services, Inc
01.11.2018
|
Subjects | |
Online Access | Get full text |
ISSN | 0021-9541 1097-4652 1097-4652 |
DOI | 10.1002/jcp.26536 |
Cover
Summary: | As a major cause of renal failure, transient renal ischemia and reperfusion induce both acute kidney injury and late fibrosis, which are the common pathological manifestations of end‐stage renal disease. Curcumin is a biologically active polyphenolic compound found in turmeric. Increasing evidence has demonstrated that curcumin has a protective action against renal fibrosis, whereas mechanisms underlying the anti‐fibrosis role of curcumin remain poorly defined. Here, we found that APPL1, an important intracellular binding partner for AdipoR, was involved in the pathogenesis of acute injury or fibrosis and was significantly upregulated by curcumin in a mouse model of ischemia reperfusion‐induced late kidney fibrosis. Moreover, Akt signaling was the specific signaling pathway identified downstream of APPL1 in the pathogenesis of fibrosis. Our in vitro experiment demonstrated that curcumin alleviates ischemia reperfusion‐induced late kidney fibrosis via the APPL1/Akt pathway. These data are helpful for understanding the anti‐fibrosis mechanism of curcumin in the pathogenesis of AKI‐induced late fibrosis.
The present study aimed to investigate whether curcumin exhibited a protective effect on ischemia reperfusion‐induced late kidney fibrosis by activating APPL1 via the Akt phosphorylation pathway. |
---|---|
Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 |
ISSN: | 0021-9541 1097-4652 1097-4652 |
DOI: | 10.1002/jcp.26536 |