β-catenin deficiency in renal fibroblasts induces HGF expression and activates tyrosine phosphorylation of the c-met receptor after IRI, thereby promoting cell proliferation and renal repair.70 In injured kidneys, proHGF is processed and cleaved to form mature HGF that binds to the c-met receptor.62 Conditional knockout of c-met in renal tubules exacerbates renal injury and inhibits renal regeneration after AKI. Here, HGF is linked to acute kidney injury.