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Year : 2021  |  Volume : 8  |  Issue : 1  |  Page : 10

JUN amino terminal kinase in cell death and inflammation in acute and chronic kidney disease

Department of Nephrology, Monash Medical Centre; Monash University Centre for Inflammatory Diseases, Monash Medical Centre, Clayton, Victoria, Australia

Correspondence Address:
Prof. David J Nikolic-Paterson
Department of Nephrology, Monash Medical Centre, Clayton, Victoria 3168
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/imna.imna_35_21

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Cell death and inflammation are important mechanisms in the induction of acute kidney injury (AKI) and the progression of chronic kidney disease. This focused review examines how the JUN amino terminal kinase (JNK) enzyme contributes to these pathologies. The JNK enzyme is activated in response to cellular stress, being most sensitive to oxidative stress. Biopsy studies have shown that JNK signaling is activated in human AKI and chronic kidney injury. Genetic and pharmacologic strategies have demonstrated a key role for JNK signaling in tubular cell death, inflammation, and loss of renal function in various animal models of AKI. This has been directly attributed to JNK1 signaling in the proximal tubular epithelial cells. JNK inhibition also reduces cell death, inflammation, and fibrosis in several models of progressive kidney disease; however, not all models show benefit with JNK blockade. JNK inhibitors are currently in clinical trials which opens the way for testing JNK-based therapy in selected types of renal injury. Some of the outstanding questions in this field include identifying the JNK1 target(s) in the induction of tubular cell necroptosis, and determining whether the pro-inflammatory actions of JNK signalling depend solely upon activation of JUN/Activator Protein-1.

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