Dehydroepiandrosterone Suppresses Keloid Fibroblasts Fibrosis by Inhibiting the TGF-β1/Smad Signaling Pathway.

The pathogenesis of keloid is complex and unclear, and current therapies of this condition remain unsatisfactory. Dehydroepiandrosterone (DHEA), a steroid prohormone, exhibits a wide range of pharmacologic activities, including anti-inflammatory and pro-immune effects, as well as anti-tumor and anti-fibrotic properties. Herein, the authors explored the potential effects and underlying mechanisms of DHEA on keloid fibroblasts in vitro. The authors' findings indicated that DHEA significantly inhibited the proliferation, migration, and invasion of keloid fibroblasts, while promoting cell apoptosis. In addition, DHEA significantly reduced the expression of fibrosis-related proteins in keloid fibroblasts by suppressing the TGF-β1/Smad signaling pathway. In conclusion, the authors' in vitro results highlight the therapeutic potential of DHEA as a promising candidate for keloid treatment.