Targeting protein translation to prevent septic kidney injury
Sarah C. Huen
Departments of Internal Medicine-Nephrology and Pharmacology, University of Texas Southwestern Medical Center, Dallas, Texas, USA.
Address correspondence to: Sarah C. Huen, 5323 Harry Hines Blvd., Dallas, Texas 75390-9041, USA. Phone: 214.645.8017; Email: Sarah.Huen@UTSouthwestern.edu.
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First published December 3, 2018 - More info
J Clin Invest. 2019;129(1):60–62. https://doi.org/10.1172/JCI125432.
Copyright © 2019, American Society for Clinical Investigation
The development of acute kidney injury (AKI) in patients with sepsis causes significant morbidity and mortality. The pathogenesis of AKI in sepsis is incompletely understood. In this issue of the JCI, Hato et al. investigate the renal translatome during bacterial sepsis and identify the global shutdown of renal protein translation mediated by the eukaryotic translation initiation factor 2-α kinase 2/eukaryotic translation initiation factor 2α (EIF2AK2/eIF2α) axis as a major pathway in mediating septic AKI. The results of this study suggest that inhibiting this pathway could be a potential therapeutic strategy for preventing septic AKI.
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