SPP1 and renal fibrosis: Deletion of β-catenin in macrophages attenuated the ECM deposition and renal inflammation by limiting M2 macrophage polarization.375 Overexpression of Wnt9a drove tubular senescence and produce TGF-β1, which promoted proliferation and activation in normal rat kidney fibroblasts.376 Tubule-derived Wnts but not fibroblasts-derived Wnts were necessary for fibroblasts activation and renal fibrosis.377 Moreover, β-catenin expressed by TECs controlled the release of osteopontin (OPN) enriched exosome which promoted fibroblast proliferation and activation by binding to CD44.340