Please use this identifier to cite or link to this item:
Title: Balancing the energy equation for healthy kidneys.
Austin Authors: Mount, Peter F ;Power, David Anthony
Affiliation: Department of Nephrology, Austin Health, Heidelberg, Victoria, Australia
Institute for Breathing and Sleep, Austin Health, Heidelberg, Victoria, Australia
Department of Medicine, University of Melbourne, Parkville, Melbourne, Australia
Issue Date: Dec-2015 2015-09-10
Publication information: The Journal of pathology 2015; 237(4): 407-410
Abstract: The high-energy requirement of the kidney and the importance of energy metabolism in renal physiology has been appreciated for decades, but only recently has there emerged a strong link between impaired renal energy metabolism and chronic kidney disease (CKD). The mechanisms underlying the association between changes in energy metabolism and progression of CKD, however, remain poorly understood. A new study from Qiu and colleagues reported in the Journal of Pathology has advanced this understanding by showing that, after renal injury, the energy sensor AMPK inhibits epithelial-mesenchymal transition and inflammation, processes important in the pathogenesis of CKD. Furthermore, this study identifies an interaction between AMPK and CK2β as an important mechanism in the anti-fibrotic effect. CK2β has previously been shown to interact with STK11 (also known as LKB1) to regulate cellular polarity. These findings are consistent with the known roles of the LKB1-AMPK pathway in sustaining cellular energy homeostasis and epithelial cell polarity, and add to growing evidence linking the suppression of energy metabolism to CKD. They emphasize the importance of energy metabolism in general and the LKB1-AMPK axis in particular as key investigational and therapeutic targets in the battle against CKD.
DOI: 10.1002/path.4600
ORCID: 0000-0001-7637-3661
PubMed URL: 26296948
Type: Journal Article
Subjects: AMP-activated protein kinase (AMPK)
chronic kidney disease (CKD)
epithelial-mesenchymal transition (EMT)
fatty acid oxidation (FAO)
liver kinase B1 (LKB1/STK11)
tubulo-interstitial fibrosis (TIF)
Appears in Collections:Journal articles

Show full item record

Page view(s)

checked on Dec 7, 2022

Google ScholarTM


Items in AHRO are protected by copyright, with all rights reserved, unless otherwise indicated.