A protective role for microRNA-688 in acute kidney injury

• Published in: The Journal of clinical investigation Vol. 128; no. 12; pp. 5216 - 5218
• Main Authors: Chun, Nicholas, Coca, Steven G, He, John Cijiang
• Format: Journal Article
• Language: English
• Published: United States American Society for Clinical Investigation 01.12.2018
• Subjects: Acute kidney failure; Acute Kidney Injury; Animals; Apoptosis; Biochemistry; Care and treatment; Cell death; Humans; Ischemia; Medical schools; Mice; MicroRNA; MicroRNAs; Mitochondrial Dynamics; Mitochondrial Proteins; Reperfusion Injury
• ISSN: 0021-9738; 1558-8238
• DOI: 10.1172/JCI124923

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.