Abstract
Background: Chronic kidney disease (CKD) is a condition increasingly affecting millions of individuals worldwide and is ranked as the ninth leading cause of death in the United States. AMPactivated protein kinase (AMPK) is an energy sensor that plays a pivotal role in cellular homoeostasis. Deficiency in AMPK activity and autophagic signaling, and sustained activation of mammalian target of rapamycin (mTOR) signaling and endoplasmic reticulum (ER) stress have been shown to promote epithelial-to-mesenchymal transition (EMT) and renal cell apoptosis and contribute to CKD. Emerging evidences demonstrate that AMPK acts as a modulator of the aforementioned pathways that underpin the pathophysiology of CKD. Furthermore, pharmacological activators of AMPK such as metformin have been shown to exert renoprotective effects in experimental studies and improve clinical outcomes in patients with CKD.
Objective: The current review focuses on the nephroprotective effects of AMPK and its utility as a therapeutic target for the prevention and treatment of CKD.
Keywords: AMP-activated protein kinase, apoptosis, autophagy, chronic kidney disease, endoplasmic reticulum stress, epithelial- mesenchymal transition, mammalian target of rapamycin, metformin.
Current Drug Targets
Title:AMP-activated Protein Kinase as a Drug Target in Chronic Kidney Disease
Volume: 19 Issue: 6
Author(s): Soumaya Allouch and Shankar Munusamy*
Affiliation:
- College of Pharmacy, Qatar University, PO Box 2713, Doha,Qatar
Keywords: AMP-activated protein kinase, apoptosis, autophagy, chronic kidney disease, endoplasmic reticulum stress, epithelial- mesenchymal transition, mammalian target of rapamycin, metformin.
Abstract: Background: Chronic kidney disease (CKD) is a condition increasingly affecting millions of individuals worldwide and is ranked as the ninth leading cause of death in the United States. AMPactivated protein kinase (AMPK) is an energy sensor that plays a pivotal role in cellular homoeostasis. Deficiency in AMPK activity and autophagic signaling, and sustained activation of mammalian target of rapamycin (mTOR) signaling and endoplasmic reticulum (ER) stress have been shown to promote epithelial-to-mesenchymal transition (EMT) and renal cell apoptosis and contribute to CKD. Emerging evidences demonstrate that AMPK acts as a modulator of the aforementioned pathways that underpin the pathophysiology of CKD. Furthermore, pharmacological activators of AMPK such as metformin have been shown to exert renoprotective effects in experimental studies and improve clinical outcomes in patients with CKD.
Objective: The current review focuses on the nephroprotective effects of AMPK and its utility as a therapeutic target for the prevention and treatment of CKD.
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Cite this article as:
Allouch Soumaya and Munusamy Shankar *, AMP-activated Protein Kinase as a Drug Target in Chronic Kidney Disease, Current Drug Targets 2018; 19 (6) . https://dx.doi.org/10.2174/1389450118666170601130947
DOI https://dx.doi.org/10.2174/1389450118666170601130947 |
Print ISSN 1389-4501 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5592 |
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