AbstractKidney injury is a common complication of severe disease. Here, we report that injuries of the zebrafish embryonal kidney are rapidly repaired by a migratory response in 2-, but not in 1-day-old embryos. Gene expression profiles between these two developmental stages identifycxcl12aandmycaas candidates involved in the repair process. Zebrafish embryos withcxcl12a,cxcr4b, ormycadeficiency display repair abnormalities, confirming their role in response to injury. In mice with a kidney-specific knockout,Cxcl12andMycgene deletions suppress mitochondrial metabolism and glycolysis, and delay the recovery after ischemia/reperfusion injury. Probing these observations in zebrafish reveal that inhibition of glycolysis slows fast migrating cells and delays the repair after injury, but does not affect the slow cell movements during kidney development. Our findings demonstrate thatCxcl12andMycfacilitate glycolysis to promote fast migratory responses during development and repair, and potentially also during tumor invasion and metastasis.