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.
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