Mitochondrial dysfunction is the most prominent source of oxidative stress in acute and
chronic kidney disease. NLRX1 is a receptor of the innate immune system that is
ubiquitously expressed and localized in mitochondria. We investigated whether NLRX1 may
act at the interface of metabolism and innate immunity in a model of oxidative stress. Using a
chimeric mouse model for renal ischemia-reperfusion injury, we found that NLRX1 protects
against mortality, mitochondrial damage, and epithelial cell apoptosis in an oxidative stress …