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The TGF-β/Smad3 pathway: radiation damage results in TGF-β1 release from endothelial cells, fibroblasts, and keratinocytes. TGF-β1 binds the TβRII, which becomes phosphorylated and recruits the TβRI receptor. TβRI then phosphorylates the receptor associated Smads, Smad2, and Smad3, which bind Smad4, the common mediator. The receptor Smads and the common mediator form a complex, which translocates to the nucleus and acts as a transcription factor for a number of pro-fibrotic genes.
