CXCL12 and MYC control energy metabolism to support adaptive responses after kidney injury

  • Toma A Yakulov
  • Abhijeet P Todkar
  • Krasimir Slanchev
  • Johannes Wiegel
  • Alexandra Bona
  • Martin Groß
  • Alexander Scholz
  • Isabell Hess
  • Anne Wurditsch
  • Florian Grahammer
  • Tobias B Huber
  • Virginie Lecaudey
  • Tillmann Bork
  • Jochen Hochrein
  • Melanie Boerries
  • Justine Leenders
  • Pascal de Tullio
  • François Jouret
  • Albrecht Kramer-Zucker
  • Gerd Walz

Related Research units


Kidney 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 identify cxcl12a and myca as candidates involved in the repair process. Zebrafish embryos with cxcl12a, cxcr4b, or myca deficiency display repair abnormalities, confirming their role in response to injury. In mice with a kidney-specific knockout, Cxcl12 and Myc gene 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 that Cxcl12 and Myc facilitate glycolysis to promote fast migratory responses during development and repair, and potentially also during tumor invasion and metastasis.

Bibliographical data

Original languageEnglish
Publication statusPublished - 10.09.2018
PubMed 30202007