Mind the gap: renal tubule responses to injury and the role of Cxcl12 and Myc

Acute kidney injury (AKI) is a common disorder resulting from multi-factorial ischemic, toxic and septic insults to the kidney (1,2). A common feature of all of these injuries is that there is often a profound reduction in renal blood flow resulting in tissue hypoxia. Therapeutic options are limited and there is considerable interest in understanding the response of the kidney to injury so that better interventions can be developed. In a study published in Nature Communications, Yakulov et al. utilize zebrafish and mouse models of AKI to show that the renal tubules undergo a metabolic switch to glycolysis as an adaptive and protective response to injury. By studying genetic knockouts and transgenic animals, combined with RNA-Seq, they implicate the chemokine ligand Cxcl12 (aka Sdf1) and its G protein-coupled receptor Cxcr4, as well as the proto-oncogene Myc, as key responders to injury and potential drivers of metabolic reprogramming (3)