This invention is based, at least in part, on the discovery that kidney injury results in an up-regulation of Wnt ligands in macrophages and the canonical Wnt response in epithelial cells. While macrophages from the injured kidney are a source of increased Wnt activity, compromise of Wnt receptors or conditional deletion of Wnt7b in the macrophage lineage results in a reduction of the repair response and persistent injury.
Macrophage Wnt7b is required for repair of the kidney tubule basal lamina and relief of a G2 arrest in kidney epithelial cells. The method provides for a therapeutic compound that enhances canonical Wnt signaling in epithelial cells.