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

Abstract

Kidney disease: drug target for acute injury following reperfusion Inhibition of a metabolic enzyme linked to inflammation could be a novel treatment approach for sudden kidney failure following a “reperfusion” injury caused by blood flow returning to the organ after a period of insufficient blood supply. Damian Mole and colleagues from the University of Edinburgh, UK, temporarily blocked blood vessels leading to the kidneys of mice to induce organ damage. Mice that lacked a working copy of kynurenine 3-monooxygenase (KMO), a gene that encodes an enzyme involved in metabolizing an essential amino acid linked to immune activation, were protected from injury. These KMO-mutant mice experienced less damage to the kidney’s tubular cells and had fewer pro-inflammatory cells than genetically normal animals. The findings support the idea that blocking KMO and its associated metabolic pathway could help mitigate kidney damage following reperfusion injury in humans.