Commentary 10.1172/JCI125432

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.

Find articles by Huen, S. in: JCI | PubMed | Google Scholar

First published December 3, 2018 - More info

Published in Volume 129, Issue 1 on January 2, 2019
J Clin Invest. 2019;129(1):60–62. https://doi.org/10.1172/JCI125432.
Copyright © 2019, American Society for Clinical Investigation
First published December 3, 2018 - Version history

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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