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Updated: Feb 5, 2026
Controlled Cervical Laceration Injury in Mice
Published on: May 9, 2013
CXCL12 and MYC control energy metabolism to support adaptive responses after kidney injury
Toma A Yakulov1, Abhijeet P Todkar1, Krasimir Slanchev1,2
1Renal Division, University Freiburg Medical Center, Faculty of Medicine, University of Freiburg, Hugstetter Strasse 55, 79106, Freiburg, Germany.
Abstract:
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.
Insights
Severe kidney injury repair in zebrafish is facilitated by Cxcl12 and Myc, which promote cell migration through glycolysis. This finding highlights potential therapeutic targets for kidney repair and cancer metastasis.
Area of Science:
- Developmental Biology
- Renal Physiology
- Molecular Biology
Background:
- Kidney injury is a frequent complication of severe diseases.
- Zebrafish embryos exhibit developmental stage-dependent kidney repair capabilities.
Purpose of the Study:
- To investigate the molecular mechanisms underlying kidney injury repair in zebrafish embryos.
- To identify key genes and metabolic pathways involved in kidney repair.
Main Methods:
- Comparative gene expression profiling of zebrafish embryos at different developmental stages.
- Functional analysis of candidate genes (cxcl12a, myca) using knockout models.
- Investigation of metabolic pathways, specifically glycolysis, in relation to cell migration and repair.
- Utilizing mouse models with kidney-specific gene deletions to study injury recovery.
Main Results:
- Zebrafish embryos show rapid kidney repair via migratory response at 2 days post-fertilization, but not at 1 day.
- Gene expression analysis identified cxcl12a and myca as crucial for kidney repair.
- Deficiency in cxcl12a, cxcr4b, or myca impaired zebrafish kidney repair.
- Cxcl12 and Myc gene deletion in mice suppressed mitochondrial metabolism and glycolysis, delaying recovery from ischemia/reperfusion injury.
- Inhibition of glycolysis in zebrafish slowed cell migration and delayed kidney repair.
Conclusions:
- Cxcl12 and Myc are essential for promoting fast migratory responses during kidney development and injury repair.
- These proteins facilitate glycolysis, which is critical for rapid cell migration.
- The findings suggest potential roles for Cxcl12 and Myc in tumor invasion and metastasis.
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