TGFβ2 and TGFβ3 Isoforms Drive Fibrotic Disease Pathogenesis

Researchers showed that the latent forms of TGFβ2 and TGFβ3 can be activated by integrin-independent mechanisms and have lower activation thresholds compared to TGFβ1. Unlike TGFB1, TGFB2 and TGFB3 expression was increased in human lung and liver fibrotic tissues compared to healthy control tissues.