DKK3 in keratinocytes orchestrates radiation-induced skin hyperplasia, dermatitis, and fibrosis. Radiation-induced reactive oxygen species (ROS) increase DKK3 expression in keratinocytes, which subsequently activates canonical Wnt signaling through autocrine TGF-β signaling. Elevated DKK3 levels in keratinocytes drive hyperproliferation and hyperplasia, promoting the polarization of macrophages toward a profibrotic phenotype. These polarized macrophages, in turn, upregulate..