A protective role for microRNA-688 in acute kidney injury
Nicholas Chun,1 Steven G. Coca,1 and John Cijiang He1,2
1Department of Medicine/Nephrology, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
2Renal Section, James J. Peters Veterans Affair Medical Center, New York, New York, USA.
Address correspondence to: John Cijiang He, Division of Nephrology, Box 1243, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, New York, New York 10029, USA. Phone: 212.659.1703; Email: cijiang.he@mssm.edu.
Find articles by Chun, N. in: JCI | PubMed | Google Scholar
1Department of Medicine/Nephrology, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
2Renal Section, James J. Peters Veterans Affair Medical Center, New York, New York, USA.
Address correspondence to: John Cijiang He, Division of Nephrology, Box 1243, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, New York, New York 10029, USA. Phone: 212.659.1703; Email: cijiang.he@mssm.edu.
Find articles by Coca, S. in: JCI | PubMed | Google Scholar
1Department of Medicine/Nephrology, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
2Renal Section, James J. Peters Veterans Affair Medical Center, New York, New York, USA.
Address correspondence to: John Cijiang He, Division of Nephrology, Box 1243, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, New York, New York 10029, USA. Phone: 212.659.1703; Email: cijiang.he@mssm.edu.
Find articles by He, J. in: JCI | PubMed | Google Scholar
First published November 12, 2018 - More info
J Clin Invest. 2018;128(12):5216–5218. https://doi.org/10.1172/JCI124923.
Copyright © 2018, American Society for Clinical Investigation
Ischemia-reperfusion (I/R) sets off a devastating cascade of events, leading to cell death and possible organ failure. Treatments to limit I/R-associated damage are lacking, and the pathways that drive injury are poorly understood. In this issue of the JCI, Wei and colleagues identify microRNA-668 (miR-668) as a protective factor in acute kidney injury (AKI). miR-668 was shown to repress mitochondrial fission–associated protein MTP18, thereby inhibiting pathogenic mitochondrial fragmentation. In murine models of I/R-induced AKI, treatment with a miR-668 mimetic reduced mitochondrial fragmentation and improved renal function. Moreover, HIF-1α was shown to be required for miR-688 expression in response to I/R. Importantly, Wei et al. show miR-668 upregulation in a cohort of human patients with AKI. Together, these results identify a HIF-1α/miR-668/MTP18 axis that may have potential as a therapeutic target for AKI.
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ISSN: 0021-9738 (print), 1558-8238 (online)