Kynurenine 3-monooxygenase is a critical regulator of renal ischemia–reperfusion injury

Xiaozhong Zheng, Ailiang Zhang, Margaret Binnie, Kris McGuire, Scott Webster, Jeremy Hughes, Sarah E M Howie, Damian Mole

Research output: Contribution to journalArticlepeer-review

Abstract / Description of output

Acute kidney injury (AKI) following ischemia-reperfusion injury (IRI) has a high mortality and lacks specific therapies. Here, we report that mice lacking kynurenine 3-monooxygenase (KMO) activity (Kmonull mice) are protected against AKI after renal IRI. We show that KMO is highly expressed in the kidney and exerts major metabolic control over the biologically-active kynurenine metabolites 3-hydroxykynurenine, kynurenic acid and downstream metabolites. In experimental AKI induced by kidney IRI, Kmonull mice had preserved renal function, reduced renal tubular cell injury, and fewer infiltrating neutrophils compared to wild-type (Kmowt) control mice. Together, these data confirm that flux through KMO contributes to AKI after IRI, and supports the rationale for KMO inhibition as a therapeutic strategy to protect against AKI during critical illness.
Original languageEnglish
Article number15
JournalExperimental & Molecular Medicine (EMM)
Early online date13 Feb 2019
Publication statusE-pub ahead of print - 13 Feb 2019


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