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Comment
. 2019 Jan 2;129(1):60-62.
doi: 10.1172/JCI125432. Epub 2018 Dec 3.

Targeting protein translation to prevent septic kidney injury

Sarah C Huen
Comment

Targeting protein translation to prevent septic kidney injury

Sarah C Huen. J Clin Invest. .

Abstract

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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Conflict of interest statement

Conflict of interest: The author has declared that no conflict of interest exists.

Figures

Figure 1
Figure 1. Targeting the ISR in bacterial sepsis to limit kidney injury.
Inhibition of the PKR/eIF2α axis limits global renal protein translation shutdown and the development of AKI in mouse models of bacterial sepsis. Further research will be needed to determine whether systemic inhibition of ISR will deter adaptive stress responses in other organs or alter pathogen control by the immune system.
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