Going from acute to chronic kidney injury with FoxO3
Xiangchen Gu, Archana Raman, and Katalin Susztak
Department of Medicine/Nephrology, Departments of Genetics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Address correspondence to: Katalin Susztak, University of Pennsylvania, 3400 Civic Center Blvd., 12-123 Smilow Translational Research Building, Philadelphia, Pennsylvania 19104, USA. Phone: 215.898.2009; Email: ksusztak@pennmedicine.upenn.edu.
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Department of Medicine/Nephrology, Departments of Genetics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Address correspondence to: Katalin Susztak, University of Pennsylvania, 3400 Civic Center Blvd., 12-123 Smilow Translational Research Building, Philadelphia, Pennsylvania 19104, USA. Phone: 215.898.2009; Email: ksusztak@pennmedicine.upenn.edu.
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Department of Medicine/Nephrology, Departments of Genetics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Address correspondence to: Katalin Susztak, University of Pennsylvania, 3400 Civic Center Blvd., 12-123 Smilow Translational Research Building, Philadelphia, Pennsylvania 19104, USA. Phone: 215.898.2009; Email: ksusztak@pennmedicine.upenn.edu.
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First published May 6, 2019 - More info
J Clin Invest. 2019;129(6):2192–2194. https://doi.org/10.1172/JCI128985.
© 2019 American Society for Clinical Investigation
Acute kidney injury (AKI) is one of the most important risk factors for chronic and progressive kidney disease, leading to end-stage kidney failure. Tubule epithelial regeneration leads to the resolution of renal failure in AKI. Failure of tubule epithelial regeneration leads to concomitant hypoxia from loss of microcirculation, which serves as a critical factor leading to chronic kidney disease. In this issue of the JCI, Li et al. show that hypoxia activates the stress-responsive transcription factor FoxO3. Increased FoxO3 protein abundance leads to alterations in tubular epithelial autophagy and metabolism, highlighting an important mechanism causing permanent renal damage even after an acute injury.
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